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Proteintech sirt7 antibody

Impaired <t>SIRT7</t> expression and activity in vitiligo melanocytes under oxidative stress. (A) The expression of Ac-lysine and Ac-histone on PIG1 and PIG3V cells after the treatment of H 2 O 2 (750 μM) for 24 h (mean ± SEM is shown, n = 3). (B) Cell viability of PIG1 and PIG3V cells. The cells were treated with H 2 O 2 (750 μM) for 24 h and pretreated with or without Fer-1 (5 μM) or TSA (5 μM), or NAM (100 nM) for 6 h (mean ± SEM is shown, n = 3). PIG1 and PIG3V cells were treated with H 2 O 2 (750 μM) for 24 h. (C) NAD + level (mean ± SEM is shown, n = 3). (D) Relative mRNA level of SIRT1-SIRT7 (mean ± SEM is shown, n = 3). (E) Relative protein expression of SIRT7 was analyzed (mean ± SEM is shown, n = 3). (F) Western blot results of p53 and Ac-p53. Relative expression of Ac-p53/p53 was determined by Image J software (mean ± SEM is shown, n = 3). (G) Relative protein expression of Ac-H3K18 was analyzed (mean ± SEM is shown, n = 3). (H) The differentially-expression of SIRT7 in healthy skin versus perifocal skin of vitiligo based on single-cell RNA sequencing (scRNA-seq) data. (I) Representative images of melanocytes for SIRT7 in healthy skin and perilesional skin of vitiligo (mean ± SD is shown, n = 5). Melanocytes were stained with Melan-A (red) antibody. Nuclei were counterstained with DAPI (blue). Scale bar = 100 μm (Magnification the left 200 ×; right 400 × ). *P < 0.05, **P < 0.01, ***P < 0.001, ns for non-significant (one-way ANOVA and two-tailed Student’s t test). (For interpretation of the references to colour in this figure legend, the reader is referred to the web version of this article.)

Sirt7 Antibody, supplied by Proteintech, used in various techniques. Bioz Stars score: 93/100, based on 53 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Average 93 stars, based on 53 article reviews

sirt7 antibody - by Bioz Stars, 2026-10

93/100 stars

Images

1) Product Images from "SIRT7 facilitates ferroptosis resistance of melanocytes via activating the SMAD3-ATF3-GPX4 signaling pathway in vitiligo"

Article Title: SIRT7 facilitates ferroptosis resistance of melanocytes via activating the SMAD3-ATF3-GPX4 signaling pathway in vitiligo

Journal: Journal of Advanced Research

doi: 10.1016/j.jare.2025.07.020

Impaired SIRT7 expression and activity in vitiligo melanocytes under oxidative stress. (A) The expression of Ac-lysine and Ac-histone on PIG1 and PIG3V cells after the treatment of H 2 O 2 (750 μM) for 24 h (mean ± SEM is shown, n = 3). (B) Cell viability of PIG1 and PIG3V cells. The cells were treated with H 2 O 2 (750 μM) for 24 h and pretreated with or without Fer-1 (5 μM) or TSA (5 μM), or NAM (100 nM) for 6 h (mean ± SEM is shown, n = 3). PIG1 and PIG3V cells were treated with H 2 O 2 (750 μM) for 24 h. (C) NAD + level (mean ± SEM is shown, n = 3). (D) Relative mRNA level of SIRT1-SIRT7 (mean ± SEM is shown, n = 3). (E) Relative protein expression of SIRT7 was analyzed (mean ± SEM is shown, n = 3). (F) Western blot results of p53 and Ac-p53. Relative expression of Ac-p53/p53 was determined by Image J software (mean ± SEM is shown, n = 3). (G) Relative protein expression of Ac-H3K18 was analyzed (mean ± SEM is shown, n = 3). (H) The differentially-expression of SIRT7 in healthy skin versus perifocal skin of vitiligo based on single-cell RNA sequencing (scRNA-seq) data. (I) Representative images of melanocytes for SIRT7 in healthy skin and perilesional skin of vitiligo (mean ± SD is shown, n = 5). Melanocytes were stained with Melan-A (red) antibody. Nuclei were counterstained with DAPI (blue). Scale bar = 100 μm (Magnification the left 200 ×; right 400 × ). *P < 0.05, **P < 0.01, ***P < 0.001, ns for non-significant (one-way ANOVA and two-tailed Student’s t test). (For interpretation of the references to colour in this figure legend, the reader is referred to the web version of this article.)

Figure Legend Snippet: Impaired SIRT7 expression and activity in vitiligo melanocytes under oxidative stress. (A) The expression of Ac-lysine and Ac-histone on PIG1 and PIG3V cells after the treatment of H 2 O 2 (750 μM) for 24 h (mean ± SEM is shown, n = 3). (B) Cell viability of PIG1 and PIG3V cells. The cells were treated with H 2 O 2 (750 μM) for 24 h and pretreated with or without Fer-1 (5 μM) or TSA (5 μM), or NAM (100 nM) for 6 h (mean ± SEM is shown, n = 3). PIG1 and PIG3V cells were treated with H 2 O 2 (750 μM) for 24 h. (C) NAD + level (mean ± SEM is shown, n = 3). (D) Relative mRNA level of SIRT1-SIRT7 (mean ± SEM is shown, n = 3). (E) Relative protein expression of SIRT7 was analyzed (mean ± SEM is shown, n = 3). (F) Western blot results of p53 and Ac-p53. Relative expression of Ac-p53/p53 was determined by Image J software (mean ± SEM is shown, n = 3). (G) Relative protein expression of Ac-H3K18 was analyzed (mean ± SEM is shown, n = 3). (H) The differentially-expression of SIRT7 in healthy skin versus perifocal skin of vitiligo based on single-cell RNA sequencing (scRNA-seq) data. (I) Representative images of melanocytes for SIRT7 in healthy skin and perilesional skin of vitiligo (mean ± SD is shown, n = 5). Melanocytes were stained with Melan-A (red) antibody. Nuclei were counterstained with DAPI (blue). Scale bar = 100 μm (Magnification the left 200 ×; right 400 × ). *P < 0.05, **P < 0.01, ***P < 0.001, ns for non-significant (one-way ANOVA and two-tailed Student’s t test). (For interpretation of the references to colour in this figure legend, the reader is referred to the web version of this article.)

Techniques Used: Expressing, Activity Assay, Western Blot, Software, Single Cell, RNA Sequencing, Staining, Two Tailed Test

SIRT7 inhibited ferroptosis in melanocytes under oxidative stress. (A) and (B) Enrichment analysis of GSEA and heatmap of representative ferroptotic genes between SIRT7 and ferroptosis pathway in PIG1 cell line. (C) The cell death ratio of PIG1 with the transfection of siRNA or si-SIRT7, and the PIG1 cells were treated with H 2 O 2 (750 μM) for 24 h with the pretreatment of Fer-1 (5 μM). The SIRT7 knockdown or control PIG1 cells were treated with or without H 2 O 2 (750 μM) for 24 h. (n = 3). (D) , (E) and (F) The levels of lipid ROS, MDA, and Fe 2+ were analyzed in PIG1 cells. (n = 3). (G) and (H) The alterations of GPX4 mRNA and protein were analyzed in PIG1 cells. (I) Cellular GSH level was analyzed in PIG1 cells. (n = 3). Data were presented as mean ± SEM. *P < 0.05, **P < 0.01, ***P < 0.001 (one-way ANOVA).

Figure Legend Snippet: SIRT7 inhibited ferroptosis in melanocytes under oxidative stress. (A) and (B) Enrichment analysis of GSEA and heatmap of representative ferroptotic genes between SIRT7 and ferroptosis pathway in PIG1 cell line. (C) The cell death ratio of PIG1 with the transfection of siRNA or si-SIRT7, and the PIG1 cells were treated with H 2 O 2 (750 μM) for 24 h with the pretreatment of Fer-1 (5 μM). The SIRT7 knockdown or control PIG1 cells were treated with or without H 2 O 2 (750 μM) for 24 h. (n = 3). (D) , (E) and (F) The levels of lipid ROS, MDA, and Fe 2+ were analyzed in PIG1 cells. (n = 3). (G) and (H) The alterations of GPX4 mRNA and protein were analyzed in PIG1 cells. (I) Cellular GSH level was analyzed in PIG1 cells. (n = 3). Data were presented as mean ± SEM. *P < 0.05, **P < 0.01, ***P < 0.001 (one-way ANOVA).

Techniques Used: Transfection, Knockdown, Control

SIRT7 inhibited ferroptosis via the regulation of ATF3-GPX4 signaling . (A) RT-PCR analysis of the alteration of GPX4 in PIG1 cells with the transfection of siRNA or siATF3 under oxidative stress. (n = 3). PIG1 cells were stimulated with H 2 O 2 (750 μM) with or without SIRT7 knockdown. (B) Volcano map of differentially-expressed genes. (C) and (D) RT-PCR and immunoblotting analysis of the level of ATF3. PIG1 cells were treated with H 2 O 2 (750 μM) for 24 h after being transfected with siRNA for 24 h. (E) , (F) and (G) Cell death ratio, lipid ROS levels, and Fe 2+ contents were analyzed. (n = 3). PIG1 cells of SIRT7 knockdown were treated with H 2 O 2 (750 μM) for 6 h after being transfected with siRNA for 48 h. (H) RT-PCR analysis of the level of GPX4. (n = 3). (I) The detection of GSH level. (n = 3). (J) Transcription factor analysis of the GPX4 promoter predicted the ATF3 binding site. (K) Enrichment of ATF3 binding site to the promoter of GPX4 by ChIP analysis in PIG1 cells. (n = 3). (L) Enrichment of ATF3 to the promoter of GPX4 by ChIP analysis, and the PIG1 cells were treated with H 2 O 2 (750 μM) for 6 h with or without SIRT7 knockdown. (n = 3). Data were presented as mean ± SEM. *P < 0.05, **P < 0.01, ***P < 0.001 (one-way ANOVA and two-tailed Student’s t test).

Figure Legend Snippet: SIRT7 inhibited ferroptosis via the regulation of ATF3-GPX4 signaling . (A) RT-PCR analysis of the alteration of GPX4 in PIG1 cells with the transfection of siRNA or siATF3 under oxidative stress. (n = 3). PIG1 cells were stimulated with H 2 O 2 (750 μM) with or without SIRT7 knockdown. (B) Volcano map of differentially-expressed genes. (C) and (D) RT-PCR and immunoblotting analysis of the level of ATF3. PIG1 cells were treated with H 2 O 2 (750 μM) for 24 h after being transfected with siRNA for 24 h. (E) , (F) and (G) Cell death ratio, lipid ROS levels, and Fe 2+ contents were analyzed. (n = 3). PIG1 cells of SIRT7 knockdown were treated with H 2 O 2 (750 μM) for 6 h after being transfected with siRNA for 48 h. (H) RT-PCR analysis of the level of GPX4. (n = 3). (I) The detection of GSH level. (n = 3). (J) Transcription factor analysis of the GPX4 promoter predicted the ATF3 binding site. (K) Enrichment of ATF3 binding site to the promoter of GPX4 by ChIP analysis in PIG1 cells. (n = 3). (L) Enrichment of ATF3 to the promoter of GPX4 by ChIP analysis, and the PIG1 cells were treated with H 2 O 2 (750 μM) for 6 h with or without SIRT7 knockdown. (n = 3). Data were presented as mean ± SEM. *P < 0.05, **P < 0.01, ***P < 0.001 (one-way ANOVA and two-tailed Student’s t test).

Techniques Used: Reverse Transcription Polymerase Chain Reaction, Transfection, Knockdown, Western Blot, Binding Assay, Two Tailed Test

SIRT7 de-acetylated SMAD3 to repress ATF3 transcription . (A) Transcription factor analysis of the ATF3 promoter predicted three SMAD3 binding sites. (B) Enrichment of three SMAD3 binding sites to the promoter of ATF3 by ChIP analysis in PIG1 cells. (n = 3). (C) and (D) Co-IP and immunostaining analysis of the interaction of SMAD3 and SIRT7 in PIG1 cells. (E) IP analysis of the level of acetyl-SMAD3 in PIG1 cells treated with H 2 O 2 (750 μM) for 6 h. (F) and (G) Immunoblotting and immunostaining analysis of the expression of p-SMAD3 and cells were treated with H 2 O 2 (750 μM) for 24 h with or without SIRT7 knockdown. Scale bar = 100 μm (Magnification 630 × ). (H) RT-PCR analysis of the alteration of ATF3 in PIG1 cells with the transfection of siRNA or siSMAD3 under oxidative stress. (n = 3). (I) RT-PCR analysis of the level of ATF3 in SIRT7 knockdown-PIG1 cells with H 2 O 2 (750 μM) treatment for 6 h after being transfected with siSMAD3 or siRNA for 24 h. (n = 3). (J) Enrichment of SMAD3 to the promoter of ATF3 by ChIP analysis in PIG1 cells, and the SIRT7 knockdown-PIG1 cells were treated with H 2 O 2 (750 μM) for 6 h after being transfected with siRNA or siSMAD3 for 24 h. (n = 3). Data were presented as mean ± SEM. **P < 0.01, ***P < 0.001, ns for non-significant (one-way ANOVA and two-tailed Student’s t test).

Figure Legend Snippet: SIRT7 de-acetylated SMAD3 to repress ATF3 transcription . (A) Transcription factor analysis of the ATF3 promoter predicted three SMAD3 binding sites. (B) Enrichment of three SMAD3 binding sites to the promoter of ATF3 by ChIP analysis in PIG1 cells. (n = 3). (C) and (D) Co-IP and immunostaining analysis of the interaction of SMAD3 and SIRT7 in PIG1 cells. (E) IP analysis of the level of acetyl-SMAD3 in PIG1 cells treated with H 2 O 2 (750 μM) for 6 h. (F) and (G) Immunoblotting and immunostaining analysis of the expression of p-SMAD3 and cells were treated with H 2 O 2 (750 μM) for 24 h with or without SIRT7 knockdown. Scale bar = 100 μm (Magnification 630 × ). (H) RT-PCR analysis of the alteration of ATF3 in PIG1 cells with the transfection of siRNA or siSMAD3 under oxidative stress. (n = 3). (I) RT-PCR analysis of the level of ATF3 in SIRT7 knockdown-PIG1 cells with H 2 O 2 (750 μM) treatment for 6 h after being transfected with siSMAD3 or siRNA for 24 h. (n = 3). (J) Enrichment of SMAD3 to the promoter of ATF3 by ChIP analysis in PIG1 cells, and the SIRT7 knockdown-PIG1 cells were treated with H 2 O 2 (750 μM) for 6 h after being transfected with siRNA or siSMAD3 for 24 h. (n = 3). Data were presented as mean ± SEM. **P < 0.01, ***P < 0.001, ns for non-significant (one-way ANOVA and two-tailed Student’s t test).

Techniques Used: Binding Assay, Co-Immunoprecipitation Assay, Immunostaining, Western Blot, Expressing, Knockdown, Reverse Transcription Polymerase Chain Reaction, Transfection, Two Tailed Test

Melanocytic-specific Sirt7 knockout accelerated depigmentation of tail skin in a mouse model of vitiligo . (A) Diagram of the principle of vitiligo induction. (B) Representative whole-mount tail epidermis immunofluorescence staining images in female Sirt7 fl/fl control mice, Sirt7 fl/fl control-Vitiligo mice, and Sirt7 MCKO-Vitiligo mice induced for 30 days. Nuclei were stained with Hoechst (blue). CD8 + T cells were counterstained with CD8α (green) antibody. Melanocytes were stained with Melan-A (red) antibody. (Magnification 100 ×, scale bar = 200 μm) (n = 3). (C) The representative mouse tail images and ImageJ analysis images in female Sirt7 fl/fl control mice, Sirt7 fl/fl control-Vitiligo mice, and Sirt7 MCKO-Vitiligo mice induced for 30, 60 and 90 days. (n = 3). (D) Statistical analysis of the tail pigmentation percentages in female Sirt7 fl/fl control mice, Sirt7 fl/fl control - Vitiligo mice, and Sirt7 MCKO-Vitiligo mice induced for 30, 60 and 90 days. (n = 3). (E) Representative whole-mount tail epidermis immunofluorescence staining images in female Sirt7 fl/fl control mice, Sirt7 fl/fl control-Vitiligo mice, and Sirt7 MCKO-Vitiligo mice induced for 60 days. (n = 3). (F) Immunofluorescence images of GPX4 expression within melanocytes in female Sirt7 fl/fl control-Vitiligo mice and Sirt7 MCKO-Vitiligo mice. Nuclei (blue), Melanocytes (green), GPX4 (purple). (Magnification 200 ×, scale bar = 20 μm). (n = 3). Data were presented as mean ± SD (one-way ANOVA and two-tailed Student’s t test). (For interpretation of the references to colour in this figure legend, the reader is referred to the web version of this article.)

Figure Legend Snippet: Melanocytic-specific Sirt7 knockout accelerated depigmentation of tail skin in a mouse model of vitiligo . (A) Diagram of the principle of vitiligo induction. (B) Representative whole-mount tail epidermis immunofluorescence staining images in female Sirt7 fl/fl control mice, Sirt7 fl/fl control-Vitiligo mice, and Sirt7 MCKO-Vitiligo mice induced for 30 days. Nuclei were stained with Hoechst (blue). CD8 + T cells were counterstained with CD8α (green) antibody. Melanocytes were stained with Melan-A (red) antibody. (Magnification 100 ×, scale bar = 200 μm) (n = 3). (C) The representative mouse tail images and ImageJ analysis images in female Sirt7 fl/fl control mice, Sirt7 fl/fl control-Vitiligo mice, and Sirt7 MCKO-Vitiligo mice induced for 30, 60 and 90 days. (n = 3). (D) Statistical analysis of the tail pigmentation percentages in female Sirt7 fl/fl control mice, Sirt7 fl/fl control - Vitiligo mice, and Sirt7 MCKO-Vitiligo mice induced for 30, 60 and 90 days. (n = 3). (E) Representative whole-mount tail epidermis immunofluorescence staining images in female Sirt7 fl/fl control mice, Sirt7 fl/fl control-Vitiligo mice, and Sirt7 MCKO-Vitiligo mice induced for 60 days. (n = 3). (F) Immunofluorescence images of GPX4 expression within melanocytes in female Sirt7 fl/fl control-Vitiligo mice and Sirt7 MCKO-Vitiligo mice. Nuclei (blue), Melanocytes (green), GPX4 (purple). (Magnification 200 ×, scale bar = 20 μm). (n = 3). Data were presented as mean ± SD (one-way ANOVA and two-tailed Student’s t test). (For interpretation of the references to colour in this figure legend, the reader is referred to the web version of this article.)

Techniques Used: Knock-Out, Immunofluorescence, Staining, Control, Expressing, Two Tailed Test

Cell-Signaling:

Article Title: PRAS40 promotes colorectal cancer stemness by enhancing glycolysis through triggering PGK1 acetylation.
Article Snippet: .. Antibodies were purchased for detection of PRAS40 (2691S), PCNA (13110), PCAF (3378 T) (Cell Signaling); PGK1 (17811-1-AP), CD133 (66666-1-Ig), αTubulin (66031-1-Ig), β-Actin (66009-1-Ig), CD44 (15675-1-AP) (Proteintech); SIRT7 (ab259968), anti-phosphotryosine (ab179530) (Abcam); and panAcetyl (sc-8649)(Santa Crus Biotechnology). .. Azoxymethane (AOM), Polybrene and 2-DG were from Sigma-Aldrich; dextran sodium sulfate (DSS) was from MP Biomedicals; PU139 and anacardic acid were from TOPSCIENCE.

Article Title: PRAS40 promotes colorectal cancer stemness by enhancing glycolysis through triggering PGK1 acetylation
Article Snippet: .. Antibodies were purchased for detection of PRAS40 (2691S), PCNA (13110), PCAF (3378 T) (Cell Signaling); PGK1 (17811-1-AP), CD133 (66666-1-Ig), α-Tubulin (66031-1-Ig), β-Actin (66009-1-Ig), CD44 (15675-1-AP) (Proteintech); SIRT7 (ab259968), anti-phosphotryosine (ab179530) (Abcam); and pan-Acetyl (sc-8649)(Santa Crus Biotechnology). .. Azoxymethane (AOM), Polybrene and 2-DG were from Sigma-Aldrich; dextran sodium sulfate (DSS) was from MP Biomedicals; PU139 and anacardic acid were from TOPSCIENCE.

other:

Article Title: Colchicine inhibits vascular calcification by suppressing inflammasome activation through the enhancement of the Sirt2-PP2Ac signaling pathway
Article Snippet: Sirt7 (1:1000) , Proteintech , Cat# 12994-1-AP; RRID: AB_10644276.

Article Title: Epigenetics and Mitochondrial Biogenesis: The Role of Sirtuins in HIV Neuropathogenesis
Article Snippet: SIRT7 , Protein Tech , 12,994–1-AP , 45 kDa , 1:1000/1:500.

Incubation:

Article Title: Aprocitentan mitigates doxorubicin-induced cardiotoxicity by inhibiting cuproptosis, oxidative stress, and mitochondrial impairments via the activation of sirtuin 7.
Article Snippet: Doxorubicin (DOX) is a widely used chemotherapy drug for cancer while leads to several cardiac disorders including cardiomyopathy and heart failure.. Aprocitentan is a novel dual endothelin-1 receptor antagonist and functions as an effective antihypertensive drug for resistant hypertension.. However, the exact roles of aprocitentan in DOX-induced cardiotoxicity remains largely unclear.

Article Title: Sirt1 deficiency promotes dynamic fibroblast-to-myofibroblast transition in ligamentum flavum hypertrophy via the Smad2/3 pathway.
Article Snippet: Equal amounts of protein were separated by 10% SDS-PAGE and transferred to 0.2 μm PVDF membranes (Merck Millipore, Darmstadt, Germany). .. After blocking in 5% nonfat milk for 1 h, membranes were washed in TBST and incubated overnight at 4 ◦C with primary antibodies against α-SMA (1:2000, Proteintech), Col-I (1:2000, Invitrogen), Col-III (1:2000, Invitrogen), Sirt1(1:2000, Proteintech), Sirt4(1:1000, Proteintech), Sirt7(1:1000, Proteintech), Smad2 (1:2000, Abcam, Cambridge, UK), Smad3(1:2000, Abcam), p-Smad2 (1:1000, Abcam), p-Smad3(1:1000, Abcam), and GAPDH (1:5000, Proteintech). .. Following incubation with HRP-conjugated secondary antibodies (1:2000, Invitrogen) overnight at 4 ◦C, signals were captured with a ChemiDoc imaging system (Bio-Rad, CA, USA).

Pyrolysis Gas Chromatography:

Article Title: ASIC1a Promotes nucleus pulposus derived stem cells apoptosis through modulation of SIRT3-dependent mitochondrial redox homeostasis in intervertebral disc degeneration
Article Snippet: Following electrophoresis, proteins were transferred to PVDF membranes (Bio-Rad, Hercules, CA, USA). .. The primary antibodies utilized included ASIC1a (Huaan ER1803-33, 1:1000), SIRT1 (Huaan ER130811 , 1:1000), SIRT2 (Huaan ET1611-72, 1:1000), SIRT3 (Immunoway YT4304, 1:1000), SIRT4 (Proteintech 66543-ig, 1:20000), SIRT5 (Huaan ET1701-6, 1:1000), SIRT6 (Huaan ET1701-29, 1:1000), SIRT7 (Huaan EM1707-09, 1:1000), BAX (Proteintech 50599-2-ig, 1:5000), Bcl-2 (Proteintech 26593-1-AP, 1:2000), Active Caspase-3 (Huaan ET1602-47, 1:1000), Cytochrome C (Huaan ET1610-16, 1:1000), SOD2 (Immunoway YT5575, 1:1000), AMPK (Huaan ET1608-40, 1:4000), p-AMPK (Huaan ET1612-72, 1:1000), PGC-1α (Huaan ET1702-96, 1:1000), VDAC (Huaan ET1601-20, 1:10000), and Beta Actin (Proteintech 20536-1-AP, 1:10000). .. After incubation with the corresponding secondary antibodies and subsequent washing, BeyoECL Plus (Beyotime P0018s) was employed to develop luminescence, which was detected using an automatic chemiluminescence immunoanalyzer (Tanon 5200, China).

Blocking Assay:

Image Search Results

A FACS‐based CRISPR screen identifies SIRT7 as a transcriptional repressor of MEN1 and reveals its clinical significance in PanNETs. (A) Schematic of the FACS‐coupled pooled CRISPR–Cas9 screen in BON‐1 cells. (B) Scatter plot of CRISPR gene scores (CS) from two independent screens (Replicate 1 vs. Replicate 2); selected HDAC and sirtuin hits are indicated. (C) Representative immunoblot of MEN1 in BON‐1 cells treated with small‐molecule inhibitors targeting HDAC5, SIRT2, SIRT3, SIRT5, or SIRT7 at low (L) and high (H) doses. n = 3 independent experiments. (D) Immunoblot analysis of MEN1 protein in BON‐1 cells after individual CRISPR‐Cas9 knockout of selected HDACs and sirtuins. n = 3 independent experiments. (E) Immunoblot analysis of SIRT7 and MEN1 in BON‐1 and QGP‐1 cells after SIRT7 knockdown (SIRT7‐KD#1, SIRT7‐KD#2) and rescue by re‐expression of SIRT7 (SIRT7 Flag ) in SIRT7‐KD cells; Vector denotes empty‐vector rescue control. n = 3 independent experiments. (F) RT–qPCR analysis of MEN1 mRNA in BON‐1 and QGP‐1 cells after SIRT7 knockdown. n = 3 biologically independent samples per group. Statistics: one‐way ANOVA. (G) Luciferase reporter assay measuring MEN1 promoter activity after SIRT7 knockdown. n = 5 biologically independent samples per group. Statistics: one‐way ANOVA. (H) MEN1 promoter truncation luciferase assays in QGP‐1 cells comparing CTRL versus SIRT7‐KD across indicated promoter fragments. n = 3 biologically independent samples per construct. Statistics: one‐way ANOVA. (I) Correlation between SIRT7 and MEN1 IHC scores in a PanNET tissue microarray (TMA; n = 121). Pearson correlation: R = −0.197, p = 0.027. (J) Representative IHC images of SIRT7 in paired tumor and adjacent tissues from a PanNET cohort ( n = 70 pairs) with quantification. Images are shown at 20× and 200× magnification; scale bars are indicated in the images (200×, 100 µm). Statistics: two‐sided paired t‐test. (K) Kaplan–Meier analysis of disease‐free survival (DFS) stratified by SIRT7‐high vs SIRT7‐low expression in the PanNET TMA cohort ( n = 121); log‐rank p = 0.035. Representative IHC images for SIRT7‐high and SIRT7‐low groups are shown at 20× and 200× magnification; scale bars are indicated in the images (200×, 100 µm). Statistics: log‐rank test. Data are presented as mean ± SEM unless otherwise indicated; ns, not significant; * p < 0.05, ** p < 0.01, *** p < 0.001.

Journal: Advanced Science

Article Title: Inhibition of SIRT7 Overcomes Radioresistance in Pancreatic Neuroendocrine Tumors by Reactivating MEN1 Expression

doi: 10.1002/advs.202519824

Figure Lengend Snippet: A FACS‐based CRISPR screen identifies SIRT7 as a transcriptional repressor of MEN1 and reveals its clinical significance in PanNETs. (A) Schematic of the FACS‐coupled pooled CRISPR–Cas9 screen in BON‐1 cells. (B) Scatter plot of CRISPR gene scores (CS) from two independent screens (Replicate 1 vs. Replicate 2); selected HDAC and sirtuin hits are indicated. (C) Representative immunoblot of MEN1 in BON‐1 cells treated with small‐molecule inhibitors targeting HDAC5, SIRT2, SIRT3, SIRT5, or SIRT7 at low (L) and high (H) doses. n = 3 independent experiments. (D) Immunoblot analysis of MEN1 protein in BON‐1 cells after individual CRISPR‐Cas9 knockout of selected HDACs and sirtuins. n = 3 independent experiments. (E) Immunoblot analysis of SIRT7 and MEN1 in BON‐1 and QGP‐1 cells after SIRT7 knockdown (SIRT7‐KD#1, SIRT7‐KD#2) and rescue by re‐expression of SIRT7 (SIRT7 Flag ) in SIRT7‐KD cells; Vector denotes empty‐vector rescue control. n = 3 independent experiments. (F) RT–qPCR analysis of MEN1 mRNA in BON‐1 and QGP‐1 cells after SIRT7 knockdown. n = 3 biologically independent samples per group. Statistics: one‐way ANOVA. (G) Luciferase reporter assay measuring MEN1 promoter activity after SIRT7 knockdown. n = 5 biologically independent samples per group. Statistics: one‐way ANOVA. (H) MEN1 promoter truncation luciferase assays in QGP‐1 cells comparing CTRL versus SIRT7‐KD across indicated promoter fragments. n = 3 biologically independent samples per construct. Statistics: one‐way ANOVA. (I) Correlation between SIRT7 and MEN1 IHC scores in a PanNET tissue microarray (TMA; n = 121). Pearson correlation: R = −0.197, p = 0.027. (J) Representative IHC images of SIRT7 in paired tumor and adjacent tissues from a PanNET cohort ( n = 70 pairs) with quantification. Images are shown at 20× and 200× magnification; scale bars are indicated in the images (200×, 100 µm). Statistics: two‐sided paired t‐test. (K) Kaplan–Meier analysis of disease‐free survival (DFS) stratified by SIRT7‐high vs SIRT7‐low expression in the PanNET TMA cohort ( n = 121); log‐rank p = 0.035. Representative IHC images for SIRT7‐high and SIRT7‐low groups are shown at 20× and 200× magnification; scale bars are indicated in the images (200×, 100 µm). Statistics: log‐rank test. Data are presented as mean ± SEM unless otherwise indicated; ns, not significant; * p < 0.05, ** p < 0.01, *** p < 0.001.

Article Snippet: Membranes were probed with primary antibodies specific to the following proteins: MEN1 (BBI, Cat# D263072), SIRT7 (ABclonal, Cat# A21731), DNMT1 (ABclonal, Cat# A16729), MRE11 (ABclonal, Cat# A4222), RAD50 (ABclonal, Cat# A3078), γ ‐ H2AX (ABclonal, Cat# AP0687), Caspase‐3 and Cleaved Caspase‐3 (Proteintech, Cat# 66470‐2‐Ig), and Flag epitope tag (ABclonal, Cat# AE005).

Techniques: CRISPR, Western Blot, Knock-Out, Knockdown, Expressing, Plasmid Preparation, Control, Quantitative RT-PCR, Luciferase, Reporter Assay, Activity Assay, Construct, Microarray

SIRT7 promotes malignant phenotypes in PanNETs in vitro and in vivo in a MEN1‐dependent manner. (A) Cell viability of BON‐1 and QGP‐1 cells measured by CCK‐8 under the indicated conditions. n = 3 biologically independent experiments. Statistics: one‐way ANOVA at each time point. (B) Representative images of EdU incorporation in BON‐1 and QGP‐1 cells under the indicated conditions. Images shown as DAPI, EdU, and merged channels. Scale bar, 200 µm. (C) Quantification of EdU‐positive cells corresponding to (B). Statistics: one‐way ANOVA. n = 3 biologically independent experiments. (D) Representative flow cytometry plots for Annexin V/PI apoptosis assays in BON‐1 and QGP‐1 cells under the indicated conditions. (E) Quantification of apoptotic cells corresponding to (D). Statistics: one‐way ANOVA. n = 3 biologically independent experiments. (F) Representative colony formation images of BON‐1 and QGP‐1 cells after SIRT7 knockdown with quantification shown at right. Statistics: one‐way ANOVA. n = 3 biologically independent experiments. (G) Colony formation rescue assay in SIRT7‐depleted cells re‐expressing SIRT7 (SIRT7 Flag ) or empty vector (Vector), with quantification shown at right. Statistics: one‐way ANOVA. n = 3 biologically independent experiments. (H) Representative gross anatomy images of orthotopic pancreatic tumors in mice (red arrows) generated from BON‐1 cells, comparing NC and SIRT7‐KD groups at endpoint (week 4). (I) Representative in vivo bioluminescence imaging of orthotopic tumors derived from BON‐1 cells at week 4 post‐implantation. (J) Representative macroscopic images of excised pancreatic tumors at week 4. (K) Quantification of bioluminescence intensity corresponding to (I). Statistics: unpaired two‐sided t‐test. n = 5 mice per group. (L) Endpoint tumor burden comparing NC and SIRT7‐KD groups. Statistics: unpaired two‐sided t‐test. n = 5 mice per group. Data are presented as mean ± SEM; ns, not significant; * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001.

Journal: Advanced Science

Article Title: Inhibition of SIRT7 Overcomes Radioresistance in Pancreatic Neuroendocrine Tumors by Reactivating MEN1 Expression

doi: 10.1002/advs.202519824

Figure Lengend Snippet: SIRT7 promotes malignant phenotypes in PanNETs in vitro and in vivo in a MEN1‐dependent manner. (A) Cell viability of BON‐1 and QGP‐1 cells measured by CCK‐8 under the indicated conditions. n = 3 biologically independent experiments. Statistics: one‐way ANOVA at each time point. (B) Representative images of EdU incorporation in BON‐1 and QGP‐1 cells under the indicated conditions. Images shown as DAPI, EdU, and merged channels. Scale bar, 200 µm. (C) Quantification of EdU‐positive cells corresponding to (B). Statistics: one‐way ANOVA. n = 3 biologically independent experiments. (D) Representative flow cytometry plots for Annexin V/PI apoptosis assays in BON‐1 and QGP‐1 cells under the indicated conditions. (E) Quantification of apoptotic cells corresponding to (D). Statistics: one‐way ANOVA. n = 3 biologically independent experiments. (F) Representative colony formation images of BON‐1 and QGP‐1 cells after SIRT7 knockdown with quantification shown at right. Statistics: one‐way ANOVA. n = 3 biologically independent experiments. (G) Colony formation rescue assay in SIRT7‐depleted cells re‐expressing SIRT7 (SIRT7 Flag ) or empty vector (Vector), with quantification shown at right. Statistics: one‐way ANOVA. n = 3 biologically independent experiments. (H) Representative gross anatomy images of orthotopic pancreatic tumors in mice (red arrows) generated from BON‐1 cells, comparing NC and SIRT7‐KD groups at endpoint (week 4). (I) Representative in vivo bioluminescence imaging of orthotopic tumors derived from BON‐1 cells at week 4 post‐implantation. (J) Representative macroscopic images of excised pancreatic tumors at week 4. (K) Quantification of bioluminescence intensity corresponding to (I). Statistics: unpaired two‐sided t‐test. n = 5 mice per group. (L) Endpoint tumor burden comparing NC and SIRT7‐KD groups. Statistics: unpaired two‐sided t‐test. n = 5 mice per group. Data are presented as mean ± SEM; ns, not significant; * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001.

Techniques: In Vitro, In Vivo, CCK-8 Assay, Flow Cytometry, Knockdown, Rescue Assay, Expressing, Plasmid Preparation, Generated, Imaging, Derivative Assay

SIRT7 recruits DNMT1 to the MEN1 promoter to epigenetically silence MEN1 in PanNETs. (A) Immunoprecipitation–mass spectrometry (IP–MS) analysis in QGP‐1 cells identifies DNMT1 as a SIRT7‐interacting protein. Enrichment (sequence coverage difference) of proteins detected in anti‐SIRT7 IP versus IgG control in QGP‐1 cells; DNMT1 is highlighted. (B) Quantitative pyrosequencing of MEN1 promoter methylation in paired adjacent and tumor tissues from PanNET patients ( n = 10 pairs). Statistics: two‐sided paired t‐test. (C,D) Correlation of IHC scores in PanNET TMA (n = 121): (C) DNMT1 versus MEN1 (Pearson R = −0.177, p = 0.047) and (D) DNMT1 versus SIRT7 (Pearson R = 0.277, p = 0.0016). (E) DNMT1 IHC in paired adjacent and tumor tissues ( n = 70 pairs) with representative images and quantification. Representative images are shown at 20× and 200×; scale bar, 100 µm (200×). Statistics: two‐sided paired t‐test. (F) Kaplan–Meier analysis of disease‐free survival (DFS) stratified by DNMT1‐high versus DNMT1‐low expression in the PanNET TMA cohort ( n = 121). Representative IHC images are shown at 20× and 200×; scale bar, 100 µm (200×). Statistics: log‐rank test, p = 0.043. (G) Immunoblot analysis of MEN1 in BON‐1 and QGP‐1 cells after stable DNMT1 knockdown (DNMT1‐KD#1, DNMT1‐KD#2) versus non‐targeting control (NC). n = 3 independent experiments. (H) RT–qPCR analysis of MEN1 mRNA levels in BON‐1 and QGP‐1 cells after DNMT1 knockdown. n = 3 biologically independent samples per group. Statistics: one‐way ANOVA. (I) Representative immunofluorescence images showing nuclear co‐localization of SIRT7 and DNMT1 in BON‐1 and QGP‐1 cells. Scale bar, 10 µm. n = 3 independent experiments. (J) Co‐immunoprecipitation (Co‐IP) assays validating SIRT7–DNMT1 interaction under the indicated conditions. n = 3 independent experiments. (K) DNMT1 overexpression (DNMT1 Flag ) reverses MEN1 upregulation caused by SIRT7 knockdown in BON‐1 and QGP‐1 cells. n = 3 independent experiments. (L) Heatmap of MEN1 promoter CpG methylation (Pos. 1–9) quantified by pyrosequencing in QGP‐1 cells under the indicated conditions. Values represent methylation percentage for each CpG position. n = 3 biologically independent samples per group. (M) Schematic of ChIP–qPCR primer locations at the MEN1 promoter: P1 (−81 bp), P2 (−575 bp), and a negative control region P3. (N) ChIP–qPCR analysis of DNMT1 occupancy at MEN1 promoter regions after SIRT7 knockdown. Data are shown as % input with IgG as control. n = 3 biologically independent samples per group. Statistics: unpaired two‐sided t‐test. (O) Schematic of SIRT7 constructs used for rescue: WT, catalytically inactive ΔC (aa 364–400 deletion) and ΔN (aa 1–39 deletion). (P) ChIP–qPCR analysis of DNMT1 occupancy at the MEN1 promoter in QGP‐1 cells across the indicated rescue conditions. n = 3 biologically independent samples per group. Statistics: one‐way ANOVA. (Q) Immunoblot and RT–qPCR analysis of MEN1 and DNMT1 in QGP‐1 cells across the rescue conditions. n = 3 independent experiments. (R) Co‐immunoprecipitation analysis of the interaction between DNMT1 and SIRT7 in QGP‐1 cells under the indicated rescue conditions. n = 3 independent experiments. Statistics: one‐way ANOVA. Data are presented as mean ± SEM unless otherwise indicated; ns, not significant; * p < 0.05, ** p < 0.01, *** p < 0.001.

Journal: Advanced Science

Article Title: Inhibition of SIRT7 Overcomes Radioresistance in Pancreatic Neuroendocrine Tumors by Reactivating MEN1 Expression

doi: 10.1002/advs.202519824

Figure Lengend Snippet: SIRT7 recruits DNMT1 to the MEN1 promoter to epigenetically silence MEN1 in PanNETs. (A) Immunoprecipitation–mass spectrometry (IP–MS) analysis in QGP‐1 cells identifies DNMT1 as a SIRT7‐interacting protein. Enrichment (sequence coverage difference) of proteins detected in anti‐SIRT7 IP versus IgG control in QGP‐1 cells; DNMT1 is highlighted. (B) Quantitative pyrosequencing of MEN1 promoter methylation in paired adjacent and tumor tissues from PanNET patients ( n = 10 pairs). Statistics: two‐sided paired t‐test. (C,D) Correlation of IHC scores in PanNET TMA (n = 121): (C) DNMT1 versus MEN1 (Pearson R = −0.177, p = 0.047) and (D) DNMT1 versus SIRT7 (Pearson R = 0.277, p = 0.0016). (E) DNMT1 IHC in paired adjacent and tumor tissues ( n = 70 pairs) with representative images and quantification. Representative images are shown at 20× and 200×; scale bar, 100 µm (200×). Statistics: two‐sided paired t‐test. (F) Kaplan–Meier analysis of disease‐free survival (DFS) stratified by DNMT1‐high versus DNMT1‐low expression in the PanNET TMA cohort ( n = 121). Representative IHC images are shown at 20× and 200×; scale bar, 100 µm (200×). Statistics: log‐rank test, p = 0.043. (G) Immunoblot analysis of MEN1 in BON‐1 and QGP‐1 cells after stable DNMT1 knockdown (DNMT1‐KD#1, DNMT1‐KD#2) versus non‐targeting control (NC). n = 3 independent experiments. (H) RT–qPCR analysis of MEN1 mRNA levels in BON‐1 and QGP‐1 cells after DNMT1 knockdown. n = 3 biologically independent samples per group. Statistics: one‐way ANOVA. (I) Representative immunofluorescence images showing nuclear co‐localization of SIRT7 and DNMT1 in BON‐1 and QGP‐1 cells. Scale bar, 10 µm. n = 3 independent experiments. (J) Co‐immunoprecipitation (Co‐IP) assays validating SIRT7–DNMT1 interaction under the indicated conditions. n = 3 independent experiments. (K) DNMT1 overexpression (DNMT1 Flag ) reverses MEN1 upregulation caused by SIRT7 knockdown in BON‐1 and QGP‐1 cells. n = 3 independent experiments. (L) Heatmap of MEN1 promoter CpG methylation (Pos. 1–9) quantified by pyrosequencing in QGP‐1 cells under the indicated conditions. Values represent methylation percentage for each CpG position. n = 3 biologically independent samples per group. (M) Schematic of ChIP–qPCR primer locations at the MEN1 promoter: P1 (−81 bp), P2 (−575 bp), and a negative control region P3. (N) ChIP–qPCR analysis of DNMT1 occupancy at MEN1 promoter regions after SIRT7 knockdown. Data are shown as % input with IgG as control. n = 3 biologically independent samples per group. Statistics: unpaired two‐sided t‐test. (O) Schematic of SIRT7 constructs used for rescue: WT, catalytically inactive ΔC (aa 364–400 deletion) and ΔN (aa 1–39 deletion). (P) ChIP–qPCR analysis of DNMT1 occupancy at the MEN1 promoter in QGP‐1 cells across the indicated rescue conditions. n = 3 biologically independent samples per group. Statistics: one‐way ANOVA. (Q) Immunoblot and RT–qPCR analysis of MEN1 and DNMT1 in QGP‐1 cells across the rescue conditions. n = 3 independent experiments. (R) Co‐immunoprecipitation analysis of the interaction between DNMT1 and SIRT7 in QGP‐1 cells under the indicated rescue conditions. n = 3 independent experiments. Statistics: one‐way ANOVA. Data are presented as mean ± SEM unless otherwise indicated; ns, not significant; * p < 0.05, ** p < 0.01, *** p < 0.001.

Techniques: Immunoprecipitation, Mass Spectrometry, Protein-Protein interactions, Protein Enrichment, Sequencing, Control, Methylation, Expressing, Western Blot, Knockdown, Quantitative RT-PCR, Immunofluorescence, Co-Immunoprecipitation Assay, Over Expression, CpG Methylation Assay, ChIP-qPCR, Negative Control, Construct

SIRT7 inhibition suppresses DNA damage repair pathways and sensitizes PanNET cells to irradiation. (A) Volcano plot from RNA‐seq comparing SIRT7‐knockdown (SIRT7‐KD) versus control (NC) in QGP‐1cells, highlighting representative DNA damage response (DDR) genes. n = 3 biologically independent samples per group. (B) Gene set enrichment analysis (GSEA) showing pathway‐level changes in SIRT7‐KD versus control cells. n = 3 biologically independent samples per group. (C) GO enrichment analysis of downregulated biological processes in SIRT7‐KD cells versus controls, with DDR‐related terms highlighted. n = 3 biologically independent samples per group. (D,E) RT–qPCR validation of DDR gene expression in BON‐1 (D) and QGP‐1 (E) cells treated with vehicle (Ctrl), SIRT7 inhibitor (SIRT7i, 10 µM), irradiation (IR, 4 Gy), or the combination (IR / 4 Gy + SIRT7i / 10 µM). Cells were collected 24 h after irradiation. n = 3 biologically independent experiments. Statistics: one‐way ANOVA. (F, G) Time‐course immunoblot analysis of γ‐H2AX, RAD50, and MRE11 in BON‐1 (F) and QGP‐1 (G) cells treated with IR (4 Gy) in the absence or presence of SIRT7i (10 µM) at the indicated times (0, 1, 4, 12, 24 h). n = 3 independent experiments. (H,I) Dose‐response immunoblot analysis in BON‐1 (H) and QGP‐1 (I) cells treated with increasing concentrations of SIRT7i (0, 5, 10, 15 µM) in Control (Cas9/vector) cells or MEN1‐knockout (MEN1‐KO) cells generated by CRISPR–Cas9. n = 3 independent experiments. Data are presented as mean ± SEM unless otherwise indicated. Significance is shown in the figure; ns, not significant; * p < 0.05, ** p < 0.01, *** p < 0.001.

Journal: Advanced Science

Article Title: Inhibition of SIRT7 Overcomes Radioresistance in Pancreatic Neuroendocrine Tumors by Reactivating MEN1 Expression

doi: 10.1002/advs.202519824

Figure Lengend Snippet: SIRT7 inhibition suppresses DNA damage repair pathways and sensitizes PanNET cells to irradiation. (A) Volcano plot from RNA‐seq comparing SIRT7‐knockdown (SIRT7‐KD) versus control (NC) in QGP‐1cells, highlighting representative DNA damage response (DDR) genes. n = 3 biologically independent samples per group. (B) Gene set enrichment analysis (GSEA) showing pathway‐level changes in SIRT7‐KD versus control cells. n = 3 biologically independent samples per group. (C) GO enrichment analysis of downregulated biological processes in SIRT7‐KD cells versus controls, with DDR‐related terms highlighted. n = 3 biologically independent samples per group. (D,E) RT–qPCR validation of DDR gene expression in BON‐1 (D) and QGP‐1 (E) cells treated with vehicle (Ctrl), SIRT7 inhibitor (SIRT7i, 10 µM), irradiation (IR, 4 Gy), or the combination (IR / 4 Gy + SIRT7i / 10 µM). Cells were collected 24 h after irradiation. n = 3 biologically independent experiments. Statistics: one‐way ANOVA. (F, G) Time‐course immunoblot analysis of γ‐H2AX, RAD50, and MRE11 in BON‐1 (F) and QGP‐1 (G) cells treated with IR (4 Gy) in the absence or presence of SIRT7i (10 µM) at the indicated times (0, 1, 4, 12, 24 h). n = 3 independent experiments. (H,I) Dose‐response immunoblot analysis in BON‐1 (H) and QGP‐1 (I) cells treated with increasing concentrations of SIRT7i (0, 5, 10, 15 µM) in Control (Cas9/vector) cells or MEN1‐knockout (MEN1‐KO) cells generated by CRISPR–Cas9. n = 3 independent experiments. Data are presented as mean ± SEM unless otherwise indicated. Significance is shown in the figure; ns, not significant; * p < 0.05, ** p < 0.01, *** p < 0.001.

Techniques: Inhibition, Irradiation, RNA Sequencing, Knockdown, Control, Quantitative RT-PCR, Biomarker Discovery, Gene Expression, Western Blot, Plasmid Preparation, Knock-Out, Generated, CRISPR

$Establishment of a radioresistant BON‐1 model identifies SIRT7 as a mediator of acquired radioresistance. (A) Workflow schematic showing stepwise fractionated irradiation used to generate radioresistant BON‐1 cells (BON‐1/RR) from parental BON‐1 cells, followed by RNA‐seq profiling. (B) Representative phase‐contrast images of parental and resistant BON‐1 cells at 72 h after 4 Gy irradiation. Scale bar, 200 µm. (C) Volcano plot of differentially expressed genes (resistant vs parental BON‐1), with double‐strand break (DSB) repair genes highlighted. n = 3 biologically independent samples per group. (D) Immunoblot validation of selected DSB repair factors (RAD50, MRE11, BRCA2, POLQ, RAD51, XRCC2, FEN1, BLM, FOXM1) in parental and resistant BON‐1 cells. n = 3 independent experiments. (E) Heatmap of selected differentially expressed genes showing transcriptional upregulation in resistant cells, including SIRT7. n = 3 biologically independent samples per group. (F) Cell viability after increasing irradiation doses (0, 1, 4, 8 Gy) comparing parental vs resistant BON‐1 cells. n = 5 biologically independent experiments. Statistics: unpaired two‐sided t‐test. (G) Cell viability of parental versus resistant BON‐1 cells treated with SIRT7 inhibitor (SIRT7i; 0, 5, 10, 15 µM) in combination with 4 Gy irradiation. n = 5 biologically independent experiments. Statistics: unpaired two‐sided t‐test. (H) Representative colony formation images of parental and resistant BON‐1 cells after graded irradiation (0, 1, 4, 8 Gy). (I) Quantification of clonogenic growth shown as colony area (% of non‐irradiated control). n = 3 biologically independent experiments. Statistics: unpaired two‐sided t‐test. (J) Representative colony formation images of parental and resistant BON‐1 cells after 4 Gy irradiation combined with increasing SIRT7i doses (0, 5, 10, 15 µM). (K) Quantification of colony area (% of 0 µM control). n = 3 biologically independent experiments. Statistics: unpaired two‐sided t‐test. Data are presented as mean ± SEM unless otherwise indicated; ns, not significant; * p < 0.05, ** p < 0.01, *** p < 0.001.$

Journal: Advanced Science

Article Title: Inhibition of SIRT7 Overcomes Radioresistance in Pancreatic Neuroendocrine Tumors by Reactivating MEN1 Expression

doi: 10.1002/advs.202519824

Figure Lengend Snippet: Establishment of a radioresistant BON‐1 model identifies SIRT7 as a mediator of acquired radioresistance. (A) Workflow schematic showing stepwise fractionated irradiation used to generate radioresistant BON‐1 cells (BON‐1/RR) from parental BON‐1 cells, followed by RNA‐seq profiling. (B) Representative phase‐contrast images of parental and resistant BON‐1 cells at 72 h after 4 Gy irradiation. Scale bar, 200 µm. (C) Volcano plot of differentially expressed genes (resistant vs parental BON‐1), with double‐strand break (DSB) repair genes highlighted. n = 3 biologically independent samples per group. (D) Immunoblot validation of selected DSB repair factors (RAD50, MRE11, BRCA2, POLQ, RAD51, XRCC2, FEN1, BLM, FOXM1) in parental and resistant BON‐1 cells. n = 3 independent experiments. (E) Heatmap of selected differentially expressed genes showing transcriptional upregulation in resistant cells, including SIRT7. n = 3 biologically independent samples per group. (F) Cell viability after increasing irradiation doses (0, 1, 4, 8 Gy) comparing parental vs resistant BON‐1 cells. n = 5 biologically independent experiments. Statistics: unpaired two‐sided t‐test. (G) Cell viability of parental versus resistant BON‐1 cells treated with SIRT7 inhibitor (SIRT7i; 0, 5, 10, 15 µM) in combination with 4 Gy irradiation. n = 5 biologically independent experiments. Statistics: unpaired two‐sided t‐test. (H) Representative colony formation images of parental and resistant BON‐1 cells after graded irradiation (0, 1, 4, 8 Gy). (I) Quantification of clonogenic growth shown as colony area (% of non‐irradiated control). n = 3 biologically independent experiments. Statistics: unpaired two‐sided t‐test. (J) Representative colony formation images of parental and resistant BON‐1 cells after 4 Gy irradiation combined with increasing SIRT7i doses (0, 5, 10, 15 µM). (K) Quantification of colony area (% of 0 µM control). n = 3 biologically independent experiments. Statistics: unpaired two‐sided t‐test. Data are presented as mean ± SEM unless otherwise indicated; ns, not significant; * p < 0.05, ** p < 0.01, *** p < 0.001.

Techniques: Irradiation, RNA Sequencing, Western Blot, Biomarker Discovery, Control

SIRT7 inhibition enhances radiation‐induced DNA damage, oxidative stress, and apoptosis in PanNET cells in a MEN1‐dependent manner. (A) Immunoblot analysis of γ‐H2AX, cleaved caspase‐3, RAD50, MRE11, SIRT7, and MEN1 in BON‐1 and QGP‐1 cells treated with SIRT7 inhibitor (SIRT7i, 10 µM) and/or ionizing radiation (IR, 4 Gy). Cells were harvested 12 h post‐IR. n = 3 independent experiments. (B,C) Annexin V/PI flow cytometry apoptosis assays performed 12 h post‐IR in BON‐1 and QGP‐1 cells under the indicated treatments. n = 3 biologically independent experiments. Statistics: one‐way ANOVA. (D,E) γ‐H2AX immunofluorescence staining (D) and quantification of γ‐H2AX foci (E) in BON‐1 and QGP‐1 cells at 12 h and 24 h post‐IR under the indicated treatments. Scale bar, 10 µm. n = 3 biologically independent experiments; Statistics: one‐way ANOVA at each time point. (F, G) Comet assays in BON‐1 and QGP‐1 cells at 12 h post‐IR under the indicated treatments. Left, representative comet images; right, quantification of tail moment. n = 3 biologically independent experiments. Statistics: one‐way ANOVA. (H, I) Intracellular ROS measured by DCFH‐DA staining and flow cytometry in BON‐1 and QGP‐1 cells at 12 h post‐IR under the indicated treatments; representative histograms (H) and quantification (I) are shown. n = 3 biologically independent experiments. Statistics: one‐way ANOVA. (J,K) Colony formation assays in BON‐1 and QGP‐1 cells treated with increasing concentrations of SIRT7i (0–10 µM) with or without IR; representative colony images (J) and quantification (K) of colony area are shown. n = 3 biologically independent experiments. Statistics: one‐way ANOVA. Data are presented as mean ± SEM unless otherwise indicated. Significance is shown in the figure; ns, not significant; * p < 0.05, ** p < 0.01, *** p < 0.001.

Journal: Advanced Science

Article Title: Inhibition of SIRT7 Overcomes Radioresistance in Pancreatic Neuroendocrine Tumors by Reactivating MEN1 Expression

doi: 10.1002/advs.202519824

Figure Lengend Snippet: SIRT7 inhibition enhances radiation‐induced DNA damage, oxidative stress, and apoptosis in PanNET cells in a MEN1‐dependent manner. (A) Immunoblot analysis of γ‐H2AX, cleaved caspase‐3, RAD50, MRE11, SIRT7, and MEN1 in BON‐1 and QGP‐1 cells treated with SIRT7 inhibitor (SIRT7i, 10 µM) and/or ionizing radiation (IR, 4 Gy). Cells were harvested 12 h post‐IR. n = 3 independent experiments. (B,C) Annexin V/PI flow cytometry apoptosis assays performed 12 h post‐IR in BON‐1 and QGP‐1 cells under the indicated treatments. n = 3 biologically independent experiments. Statistics: one‐way ANOVA. (D,E) γ‐H2AX immunofluorescence staining (D) and quantification of γ‐H2AX foci (E) in BON‐1 and QGP‐1 cells at 12 h and 24 h post‐IR under the indicated treatments. Scale bar, 10 µm. n = 3 biologically independent experiments; Statistics: one‐way ANOVA at each time point. (F, G) Comet assays in BON‐1 and QGP‐1 cells at 12 h post‐IR under the indicated treatments. Left, representative comet images; right, quantification of tail moment. n = 3 biologically independent experiments. Statistics: one‐way ANOVA. (H, I) Intracellular ROS measured by DCFH‐DA staining and flow cytometry in BON‐1 and QGP‐1 cells at 12 h post‐IR under the indicated treatments; representative histograms (H) and quantification (I) are shown. n = 3 biologically independent experiments. Statistics: one‐way ANOVA. (J,K) Colony formation assays in BON‐1 and QGP‐1 cells treated with increasing concentrations of SIRT7i (0–10 µM) with or without IR; representative colony images (J) and quantification (K) of colony area are shown. n = 3 biologically independent experiments. Statistics: one‐way ANOVA. Data are presented as mean ± SEM unless otherwise indicated. Significance is shown in the figure; ns, not significant; * p < 0.05, ** p < 0.01, *** p < 0.001.

Techniques: Inhibition, Western Blot, Flow Cytometry, Immunofluorescence, Staining

The SIRT7 inhibitor 97491 enhances radiation‐induced antitumor efficacy in PanNET patient‐derived xenograft (PDX) models. (A) Schematic of the PDX study design and treatment schedule. n = 5 mice per group. (B) Representative images of excised tumors at endpoint from each group. n = 5 mice per group. (C) Tumor growth curves during the treatment period. n = 5 mice per group. Statistics: one‐way ANOVA at each timepoint. (D) Body weight monitored throughout the study. n = 5 mice per group. Statistics: one‐way ANOVA at each timepoint. (E) Representative H&E and IHC staining of tumor sections for Ki‐67, MEN1, γ‐H2AX, cleaved caspase‐3 (cleaved CASP3), MRE11, and RAD50. Images are shown at 200×; scale bar, 100 µm. (F–K) Quantification of IHC positivity (% positive cells per field) for (F) Ki‐67, (G) MEN1, (H) γ‐H2AX, (I) cleaved CASP3, (J) MRE11, and (K) RAD50. n = 5 mice per group; Statistics: one‐way ANOVA. Data are presented as mean ± SEM unless otherwise indicated. Significance is shown in the figure; ns, not significant; * p < 0.05, ** p < 0.01, *** p < 0.001.

Journal: Advanced Science

Article Title: Inhibition of SIRT7 Overcomes Radioresistance in Pancreatic Neuroendocrine Tumors by Reactivating MEN1 Expression

doi: 10.1002/advs.202519824

Figure Lengend Snippet: The SIRT7 inhibitor 97491 enhances radiation‐induced antitumor efficacy in PanNET patient‐derived xenograft (PDX) models. (A) Schematic of the PDX study design and treatment schedule. n = 5 mice per group. (B) Representative images of excised tumors at endpoint from each group. n = 5 mice per group. (C) Tumor growth curves during the treatment period. n = 5 mice per group. Statistics: one‐way ANOVA at each timepoint. (D) Body weight monitored throughout the study. n = 5 mice per group. Statistics: one‐way ANOVA at each timepoint. (E) Representative H&E and IHC staining of tumor sections for Ki‐67, MEN1, γ‐H2AX, cleaved caspase‐3 (cleaved CASP3), MRE11, and RAD50. Images are shown at 200×; scale bar, 100 µm. (F–K) Quantification of IHC positivity (% positive cells per field) for (F) Ki‐67, (G) MEN1, (H) γ‐H2AX, (I) cleaved CASP3, (J) MRE11, and (K) RAD50. n = 5 mice per group; Statistics: one‐way ANOVA. Data are presented as mean ± SEM unless otherwise indicated. Significance is shown in the figure; ns, not significant; * p < 0.05, ** p < 0.01, *** p < 0.001.

Techniques: Derivative Assay, Immunohistochemistry

The proposed working model of this study. SIRT7 recruits DNMT1 to the MEN1 promoter, leading to promoter methylation and repression of MEN1 transcription. Reduced MEN1 expression promotes MRN complex activity and efficient DNA repair following irradiation, contributing to tumor cell survival. Pharmacologic inhibition of SIRT7 restores MEN1 expression, reduces MRN complex abundance, impairs DSB repair, and enhances radiosensitivity. In addition to MEN1‐dependent regulation, SIRT7 may also modulate DNA damage responses through parallel MEN1‐independent mechanisms (e.g., ATM acetylation and chromatin accessibility changes), which converge on impaired DSB repair and tumor cell death. DSB: DNA double‐strand break.

Journal: Advanced Science

Article Title: Inhibition of SIRT7 Overcomes Radioresistance in Pancreatic Neuroendocrine Tumors by Reactivating MEN1 Expression

doi: 10.1002/advs.202519824

Figure Lengend Snippet: The proposed working model of this study. SIRT7 recruits DNMT1 to the MEN1 promoter, leading to promoter methylation and repression of MEN1 transcription. Reduced MEN1 expression promotes MRN complex activity and efficient DNA repair following irradiation, contributing to tumor cell survival. Pharmacologic inhibition of SIRT7 restores MEN1 expression, reduces MRN complex abundance, impairs DSB repair, and enhances radiosensitivity. In addition to MEN1‐dependent regulation, SIRT7 may also modulate DNA damage responses through parallel MEN1‐independent mechanisms (e.g., ATM acetylation and chromatin accessibility changes), which converge on impaired DSB repair and tumor cell death. DSB: DNA double‐strand break.

Techniques: Methylation, Expressing, Activity Assay, Irradiation, Inhibition

Journal: Journal of Advanced Research

Article Title: SIRT7 facilitates ferroptosis resistance of melanocytes via activating the SMAD3-ATF3-GPX4 signaling pathway in vitiligo

doi: 10.1016/j.jare.2025.07.020

Figure Lengend Snippet: Impaired SIRT7 expression and activity in vitiligo melanocytes under oxidative stress. (A) The expression of Ac-lysine and Ac-histone on PIG1 and PIG3V cells after the treatment of H 2 O 2 (750 μM) for 24 h (mean ± SEM is shown, n = 3). (B) Cell viability of PIG1 and PIG3V cells. The cells were treated with H 2 O 2 (750 μM) for 24 h and pretreated with or without Fer-1 (5 μM) or TSA (5 μM), or NAM (100 nM) for 6 h (mean ± SEM is shown, n = 3). PIG1 and PIG3V cells were treated with H 2 O 2 (750 μM) for 24 h. (C) NAD + level (mean ± SEM is shown, n = 3). (D) Relative mRNA level of SIRT1-SIRT7 (mean ± SEM is shown, n = 3). (E) Relative protein expression of SIRT7 was analyzed (mean ± SEM is shown, n = 3). (F) Western blot results of p53 and Ac-p53. Relative expression of Ac-p53/p53 was determined by Image J software (mean ± SEM is shown, n = 3). (G) Relative protein expression of Ac-H3K18 was analyzed (mean ± SEM is shown, n = 3). (H) The differentially-expression of SIRT7 in healthy skin versus perifocal skin of vitiligo based on single-cell RNA sequencing (scRNA-seq) data. (I) Representative images of melanocytes for SIRT7 in healthy skin and perilesional skin of vitiligo (mean ± SD is shown, n = 5). Melanocytes were stained with Melan-A (red) antibody. Nuclei were counterstained with DAPI (blue). Scale bar = 100 μm (Magnification the left 200 ×; right 400 × ). *P < 0.05, **P < 0.01, ***P < 0.001, ns for non-significant (one-way ANOVA and two-tailed Student’s t test). (For interpretation of the references to colour in this figure legend, the reader is referred to the web version of this article.)

Article Snippet: For immunoprecipitation, 5–10 μL of SMAD3 antibody (9523S, Cell Signaling Technology, MA, USA), SIRT7 antibody (12994-1-AP, Proteintech, Wuhan, China) or control IgG (30000–0-AP, Proteintech) was mixed with the protein supernatant and incubated at 4°C for 2 h. Then, 25 μL of protein A/G PLUS-Agarose (sc-2003, Santa Cruz Biotechnology, Beijing, China) was mixed with protein lysates.

Techniques: Expressing, Activity Assay, Western Blot, Software, Single Cell, RNA Sequencing, Staining, Two Tailed Test

Journal: Journal of Advanced Research

Article Title: SIRT7 facilitates ferroptosis resistance of melanocytes via activating the SMAD3-ATF3-GPX4 signaling pathway in vitiligo

doi: 10.1016/j.jare.2025.07.020

Figure Lengend Snippet: SIRT7 inhibited ferroptosis in melanocytes under oxidative stress. (A) and (B) Enrichment analysis of GSEA and heatmap of representative ferroptotic genes between SIRT7 and ferroptosis pathway in PIG1 cell line. (C) The cell death ratio of PIG1 with the transfection of siRNA or si-SIRT7, and the PIG1 cells were treated with H 2 O 2 (750 μM) for 24 h with the pretreatment of Fer-1 (5 μM). The SIRT7 knockdown or control PIG1 cells were treated with or without H 2 O 2 (750 μM) for 24 h. (n = 3). (D) , (E) and (F) The levels of lipid ROS, MDA, and Fe 2+ were analyzed in PIG1 cells. (n = 3). (G) and (H) The alterations of GPX4 mRNA and protein were analyzed in PIG1 cells. (I) Cellular GSH level was analyzed in PIG1 cells. (n = 3). Data were presented as mean ± SEM. *P < 0.05, **P < 0.01, ***P < 0.001 (one-way ANOVA).

Techniques: Transfection, Knockdown, Control

Journal: Journal of Advanced Research

Article Title: SIRT7 facilitates ferroptosis resistance of melanocytes via activating the SMAD3-ATF3-GPX4 signaling pathway in vitiligo

doi: 10.1016/j.jare.2025.07.020

Figure Lengend Snippet: SIRT7 inhibited ferroptosis via the regulation of ATF3-GPX4 signaling . (A) RT-PCR analysis of the alteration of GPX4 in PIG1 cells with the transfection of siRNA or siATF3 under oxidative stress. (n = 3). PIG1 cells were stimulated with H 2 O 2 (750 μM) with or without SIRT7 knockdown. (B) Volcano map of differentially-expressed genes. (C) and (D) RT-PCR and immunoblotting analysis of the level of ATF3. PIG1 cells were treated with H 2 O 2 (750 μM) for 24 h after being transfected with siRNA for 24 h. (E) , (F) and (G) Cell death ratio, lipid ROS levels, and Fe 2+ contents were analyzed. (n = 3). PIG1 cells of SIRT7 knockdown were treated with H 2 O 2 (750 μM) for 6 h after being transfected with siRNA for 48 h. (H) RT-PCR analysis of the level of GPX4. (n = 3). (I) The detection of GSH level. (n = 3). (J) Transcription factor analysis of the GPX4 promoter predicted the ATF3 binding site. (K) Enrichment of ATF3 binding site to the promoter of GPX4 by ChIP analysis in PIG1 cells. (n = 3). (L) Enrichment of ATF3 to the promoter of GPX4 by ChIP analysis, and the PIG1 cells were treated with H 2 O 2 (750 μM) for 6 h with or without SIRT7 knockdown. (n = 3). Data were presented as mean ± SEM. *P < 0.05, **P < 0.01, ***P < 0.001 (one-way ANOVA and two-tailed Student’s t test).

Techniques: Reverse Transcription Polymerase Chain Reaction, Transfection, Knockdown, Western Blot, Binding Assay, Two Tailed Test

Journal: Journal of Advanced Research

Article Title: SIRT7 facilitates ferroptosis resistance of melanocytes via activating the SMAD3-ATF3-GPX4 signaling pathway in vitiligo

doi: 10.1016/j.jare.2025.07.020

Figure Lengend Snippet: SIRT7 de-acetylated SMAD3 to repress ATF3 transcription . (A) Transcription factor analysis of the ATF3 promoter predicted three SMAD3 binding sites. (B) Enrichment of three SMAD3 binding sites to the promoter of ATF3 by ChIP analysis in PIG1 cells. (n = 3). (C) and (D) Co-IP and immunostaining analysis of the interaction of SMAD3 and SIRT7 in PIG1 cells. (E) IP analysis of the level of acetyl-SMAD3 in PIG1 cells treated with H 2 O 2 (750 μM) for 6 h. (F) and (G) Immunoblotting and immunostaining analysis of the expression of p-SMAD3 and cells were treated with H 2 O 2 (750 μM) for 24 h with or without SIRT7 knockdown. Scale bar = 100 μm (Magnification 630 × ). (H) RT-PCR analysis of the alteration of ATF3 in PIG1 cells with the transfection of siRNA or siSMAD3 under oxidative stress. (n = 3). (I) RT-PCR analysis of the level of ATF3 in SIRT7 knockdown-PIG1 cells with H 2 O 2 (750 μM) treatment for 6 h after being transfected with siSMAD3 or siRNA for 24 h. (n = 3). (J) Enrichment of SMAD3 to the promoter of ATF3 by ChIP analysis in PIG1 cells, and the SIRT7 knockdown-PIG1 cells were treated with H 2 O 2 (750 μM) for 6 h after being transfected with siRNA or siSMAD3 for 24 h. (n = 3). Data were presented as mean ± SEM. **P < 0.01, ***P < 0.001, ns for non-significant (one-way ANOVA and two-tailed Student’s t test).

Techniques: Binding Assay, Co-Immunoprecipitation Assay, Immunostaining, Western Blot, Expressing, Knockdown, Reverse Transcription Polymerase Chain Reaction, Transfection, Two Tailed Test

Journal: Journal of Advanced Research

Article Title: SIRT7 facilitates ferroptosis resistance of melanocytes via activating the SMAD3-ATF3-GPX4 signaling pathway in vitiligo

doi: 10.1016/j.jare.2025.07.020

Figure Lengend Snippet: Melanocytic-specific Sirt7 knockout accelerated depigmentation of tail skin in a mouse model of vitiligo . (A) Diagram of the principle of vitiligo induction. (B) Representative whole-mount tail epidermis immunofluorescence staining images in female Sirt7 fl/fl control mice, Sirt7 fl/fl control-Vitiligo mice, and Sirt7 MCKO-Vitiligo mice induced for 30 days. Nuclei were stained with Hoechst (blue). CD8 + T cells were counterstained with CD8α (green) antibody. Melanocytes were stained with Melan-A (red) antibody. (Magnification 100 ×, scale bar = 200 μm) (n = 3). (C) The representative mouse tail images and ImageJ analysis images in female Sirt7 fl/fl control mice, Sirt7 fl/fl control-Vitiligo mice, and Sirt7 MCKO-Vitiligo mice induced for 30, 60 and 90 days. (n = 3). (D) Statistical analysis of the tail pigmentation percentages in female Sirt7 fl/fl control mice, Sirt7 fl/fl control - Vitiligo mice, and Sirt7 MCKO-Vitiligo mice induced for 30, 60 and 90 days. (n = 3). (E) Representative whole-mount tail epidermis immunofluorescence staining images in female Sirt7 fl/fl control mice, Sirt7 fl/fl control-Vitiligo mice, and Sirt7 MCKO-Vitiligo mice induced for 60 days. (n = 3). (F) Immunofluorescence images of GPX4 expression within melanocytes in female Sirt7 fl/fl control-Vitiligo mice and Sirt7 MCKO-Vitiligo mice. Nuclei (blue), Melanocytes (green), GPX4 (purple). (Magnification 200 ×, scale bar = 20 μm). (n = 3). Data were presented as mean ± SD (one-way ANOVA and two-tailed Student’s t test). (For interpretation of the references to colour in this figure legend, the reader is referred to the web version of this article.)

Techniques: Knock-Out, Immunofluorescence, Staining, Control, Expressing, Two Tailed Test

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