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silencing sirt7  (Vector Biolabs)


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    Vector Biolabs silencing sirt7
    Eriocitrin inhibited cuproptosis by targeting <t>SIRT7</t> to regulate the YAP/ATP7A pathway. ( A ) qPCR analysis of cuproptosis-related gene expression ( n = 8). ( B ) WB detection of protein expression after siRNA gene silencing of SIRT7 ( n = 3). ( C - D ) WB analysis of YAP/ATP7A axis ( n = 3). ( E ) qPCR analysis of cuproptosis-related gene expression ( n = 8). ( F ) WB detection of YAP expression after addition of Verteporfin ( n = 3). ( G ) WB analysis of SIRT7, ATP7A expression ( n = 3). ( H ) WB detection of protein expression after siRNA gene silencing of ATP7A ( n = 3). ( I ) WB analysis of YAP, FDX1, DLAT ( n = 3). ( J ) WB analysis of FDX1, DLAT ( n = 3). si-RNA, siRNA negative control. Verteporfin, YAP inhibitor. Data were normalized to β-actin. Data were presented as mean ± SD ( n ≥ 3 independent biological replicates). * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001
    Silencing Sirt7, supplied by Vector Biolabs, used in various techniques. Bioz Stars score: 94/100, based on 5 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Images

    1) Product Images from "Eriocitrin inhibits sodium iodate-induced cuproptosis and barrier function impairment in retinal pigment epithelium via SIRT7/YAP/ATP7A pathway"

    Article Title: Eriocitrin inhibits sodium iodate-induced cuproptosis and barrier function impairment in retinal pigment epithelium via SIRT7/YAP/ATP7A pathway

    Journal: Journal of Translational Medicine

    doi: 10.1186/s12967-025-07451-w

    Eriocitrin inhibited cuproptosis by targeting SIRT7 to regulate the YAP/ATP7A pathway. ( A ) qPCR analysis of cuproptosis-related gene expression ( n = 8). ( B ) WB detection of protein expression after siRNA gene silencing of SIRT7 ( n = 3). ( C - D ) WB analysis of YAP/ATP7A axis ( n = 3). ( E ) qPCR analysis of cuproptosis-related gene expression ( n = 8). ( F ) WB detection of YAP expression after addition of Verteporfin ( n = 3). ( G ) WB analysis of SIRT7, ATP7A expression ( n = 3). ( H ) WB detection of protein expression after siRNA gene silencing of ATP7A ( n = 3). ( I ) WB analysis of YAP, FDX1, DLAT ( n = 3). ( J ) WB analysis of FDX1, DLAT ( n = 3). si-RNA, siRNA negative control. Verteporfin, YAP inhibitor. Data were normalized to β-actin. Data were presented as mean ± SD ( n ≥ 3 independent biological replicates). * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001
    Figure Legend Snippet: Eriocitrin inhibited cuproptosis by targeting SIRT7 to regulate the YAP/ATP7A pathway. ( A ) qPCR analysis of cuproptosis-related gene expression ( n = 8). ( B ) WB detection of protein expression after siRNA gene silencing of SIRT7 ( n = 3). ( C - D ) WB analysis of YAP/ATP7A axis ( n = 3). ( E ) qPCR analysis of cuproptosis-related gene expression ( n = 8). ( F ) WB detection of YAP expression after addition of Verteporfin ( n = 3). ( G ) WB analysis of SIRT7, ATP7A expression ( n = 3). ( H ) WB detection of protein expression after siRNA gene silencing of ATP7A ( n = 3). ( I ) WB analysis of YAP, FDX1, DLAT ( n = 3). ( J ) WB analysis of FDX1, DLAT ( n = 3). si-RNA, siRNA negative control. Verteporfin, YAP inhibitor. Data were normalized to β-actin. Data were presented as mean ± SD ( n ≥ 3 independent biological replicates). * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001

    Techniques Used: Gene Expression, Expressing, Negative Control

    SIRT7 deficiency significantly impaired the protective effect of eriocitrin in alleviating NaIO₃-induced retinal barrier dysfunction and cuproptosis. ( A - B ) Western blot analysis of SIRT7 expression in mouse retinal tissue ( n = 3). ( C ) Retinal copper ion levels ( n = 7). ( D - E ) Immunofluorescence images of RPE65 in mouse retinal tissue and quantitative analysis ( n = 5). ( F - G ) Western blot analysis and quantification of YAP, ATP7A, FDX1, and DLAT protein expression ( n = 3). ( H ) qRT-PCR analysis of cuproptosis-related genes including FDX1 and DLAT ( n = 9). ( I - J ) Western blot analysis of barrier function proteins in retinal tissues ( n = 3). Scramble group: non-specific shRNA. Er: eriocitrin. Data were normalized to β-actin. Scale bar: 50 μm. Data were presented as mean ± SD ( n ≥ 3 independent biological replicates). * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001
    Figure Legend Snippet: SIRT7 deficiency significantly impaired the protective effect of eriocitrin in alleviating NaIO₃-induced retinal barrier dysfunction and cuproptosis. ( A - B ) Western blot analysis of SIRT7 expression in mouse retinal tissue ( n = 3). ( C ) Retinal copper ion levels ( n = 7). ( D - E ) Immunofluorescence images of RPE65 in mouse retinal tissue and quantitative analysis ( n = 5). ( F - G ) Western blot analysis and quantification of YAP, ATP7A, FDX1, and DLAT protein expression ( n = 3). ( H ) qRT-PCR analysis of cuproptosis-related genes including FDX1 and DLAT ( n = 9). ( I - J ) Western blot analysis of barrier function proteins in retinal tissues ( n = 3). Scramble group: non-specific shRNA. Er: eriocitrin. Data were normalized to β-actin. Scale bar: 50 μm. Data were presented as mean ± SD ( n ≥ 3 independent biological replicates). * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001

    Techniques Used: Western Blot, Expressing, Immunofluorescence, Quantitative RT-PCR, shRNA



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    Eriocitrin inhibited cuproptosis by targeting <t>SIRT7</t> to regulate the YAP/ATP7A pathway. ( A ) qPCR analysis of cuproptosis-related gene expression ( n = 8). ( B ) WB detection of protein expression after siRNA gene silencing of SIRT7 ( n = 3). ( C - D ) WB analysis of YAP/ATP7A axis ( n = 3). ( E ) qPCR analysis of cuproptosis-related gene expression ( n = 8). ( F ) WB detection of YAP expression after addition of Verteporfin ( n = 3). ( G ) WB analysis of SIRT7, ATP7A expression ( n = 3). ( H ) WB detection of protein expression after siRNA gene silencing of ATP7A ( n = 3). ( I ) WB analysis of YAP, FDX1, DLAT ( n = 3). ( J ) WB analysis of FDX1, DLAT ( n = 3). si-RNA, siRNA negative control. Verteporfin, YAP inhibitor. Data were normalized to β-actin. Data were presented as mean ± SD ( n ≥ 3 independent biological replicates). * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001
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    Image Search Results


    Eriocitrin inhibited cuproptosis by targeting SIRT7 to regulate the YAP/ATP7A pathway. ( A ) qPCR analysis of cuproptosis-related gene expression ( n = 8). ( B ) WB detection of protein expression after siRNA gene silencing of SIRT7 ( n = 3). ( C - D ) WB analysis of YAP/ATP7A axis ( n = 3). ( E ) qPCR analysis of cuproptosis-related gene expression ( n = 8). ( F ) WB detection of YAP expression after addition of Verteporfin ( n = 3). ( G ) WB analysis of SIRT7, ATP7A expression ( n = 3). ( H ) WB detection of protein expression after siRNA gene silencing of ATP7A ( n = 3). ( I ) WB analysis of YAP, FDX1, DLAT ( n = 3). ( J ) WB analysis of FDX1, DLAT ( n = 3). si-RNA, siRNA negative control. Verteporfin, YAP inhibitor. Data were normalized to β-actin. Data were presented as mean ± SD ( n ≥ 3 independent biological replicates). * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001

    Journal: Journal of Translational Medicine

    Article Title: Eriocitrin inhibits sodium iodate-induced cuproptosis and barrier function impairment in retinal pigment epithelium via SIRT7/YAP/ATP7A pathway

    doi: 10.1186/s12967-025-07451-w

    Figure Lengend Snippet: Eriocitrin inhibited cuproptosis by targeting SIRT7 to regulate the YAP/ATP7A pathway. ( A ) qPCR analysis of cuproptosis-related gene expression ( n = 8). ( B ) WB detection of protein expression after siRNA gene silencing of SIRT7 ( n = 3). ( C - D ) WB analysis of YAP/ATP7A axis ( n = 3). ( E ) qPCR analysis of cuproptosis-related gene expression ( n = 8). ( F ) WB detection of YAP expression after addition of Verteporfin ( n = 3). ( G ) WB analysis of SIRT7, ATP7A expression ( n = 3). ( H ) WB detection of protein expression after siRNA gene silencing of ATP7A ( n = 3). ( I ) WB analysis of YAP, FDX1, DLAT ( n = 3). ( J ) WB analysis of FDX1, DLAT ( n = 3). si-RNA, siRNA negative control. Verteporfin, YAP inhibitor. Data were normalized to β-actin. Data were presented as mean ± SD ( n ≥ 3 independent biological replicates). * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001

    Article Snippet: Silencing SIRT7 in mice using SIRT7 shRNA-containing adeno-associated virus (AAV), purchased from Vector Biolabs (shAAV-272012).

    Techniques: Gene Expression, Expressing, Negative Control

    SIRT7 deficiency significantly impaired the protective effect of eriocitrin in alleviating NaIO₃-induced retinal barrier dysfunction and cuproptosis. ( A - B ) Western blot analysis of SIRT7 expression in mouse retinal tissue ( n = 3). ( C ) Retinal copper ion levels ( n = 7). ( D - E ) Immunofluorescence images of RPE65 in mouse retinal tissue and quantitative analysis ( n = 5). ( F - G ) Western blot analysis and quantification of YAP, ATP7A, FDX1, and DLAT protein expression ( n = 3). ( H ) qRT-PCR analysis of cuproptosis-related genes including FDX1 and DLAT ( n = 9). ( I - J ) Western blot analysis of barrier function proteins in retinal tissues ( n = 3). Scramble group: non-specific shRNA. Er: eriocitrin. Data were normalized to β-actin. Scale bar: 50 μm. Data were presented as mean ± SD ( n ≥ 3 independent biological replicates). * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001

    Journal: Journal of Translational Medicine

    Article Title: Eriocitrin inhibits sodium iodate-induced cuproptosis and barrier function impairment in retinal pigment epithelium via SIRT7/YAP/ATP7A pathway

    doi: 10.1186/s12967-025-07451-w

    Figure Lengend Snippet: SIRT7 deficiency significantly impaired the protective effect of eriocitrin in alleviating NaIO₃-induced retinal barrier dysfunction and cuproptosis. ( A - B ) Western blot analysis of SIRT7 expression in mouse retinal tissue ( n = 3). ( C ) Retinal copper ion levels ( n = 7). ( D - E ) Immunofluorescence images of RPE65 in mouse retinal tissue and quantitative analysis ( n = 5). ( F - G ) Western blot analysis and quantification of YAP, ATP7A, FDX1, and DLAT protein expression ( n = 3). ( H ) qRT-PCR analysis of cuproptosis-related genes including FDX1 and DLAT ( n = 9). ( I - J ) Western blot analysis of barrier function proteins in retinal tissues ( n = 3). Scramble group: non-specific shRNA. Er: eriocitrin. Data were normalized to β-actin. Scale bar: 50 μm. Data were presented as mean ± SD ( n ≥ 3 independent biological replicates). * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001

    Article Snippet: Silencing SIRT7 in mice using SIRT7 shRNA-containing adeno-associated virus (AAV), purchased from Vector Biolabs (shAAV-272012).

    Techniques: Western Blot, Expressing, Immunofluorescence, Quantitative RT-PCR, shRNA

    Figure 1. SIRT7 is increased in human lung cancer tissues and cell lines. (A‑C) IHC analysis of SIRT7 in human lung cancer TMA. (A) The representative IHC images of Case 5 (tumor tissue IHC score: ‑), Case 37 (tumor tissue IHC score: +), Case 69 (tumor tissue IHC score: ++) and Case 6 (tumor tissue IHC score: +++). (B) The number of IHC scoring ‑, +, ++ or +++ cases in 102 paired lung cancer tumor/adjacent non‑tumor tissues. P<0.001, Mann‑Whitney U test. (C) The percentage of high/low SIRT7 expression in lung cancer tumor/adjacent non‑tumor tissues. *P<0.05, Pearson's χ2 test. T, tumor tissue; N, adjacent non‑tumor tissue. (D) The relative level of SIRT7 mRNA in human NSCLC cells (HBEpiC served as a control) analyzed by RT‑qPCR. (E and F) Analysis of SIRT7 protein in NSCLC cells by western blotting. (E) The representative western blot images. (F) The relative level of SIRT7 protein in NSCLC cells (HBEpiC served as a control). *P<0.05, one‑way repeated measures ANOVA with LSD post hoc multiple comparisons, n=6 per group. SIRT7, sirtuin 7; IHC, immunohistochemistry; TMS, tissue microarray; NSCLC, non‑small cell lung cancer; ANOVA, analysis of variance; LSD, least significant difference.

    Journal: Oncology reports

    Article Title: Sirtuin 7 promotes non‑small cell lung cancer progression by facilitating G1/S phase and epithelial‑mesenchymal transition and activating AKT and ERK1/2 signaling.

    doi: 10.3892/or.2020.7672

    Figure Lengend Snippet: Figure 1. SIRT7 is increased in human lung cancer tissues and cell lines. (A‑C) IHC analysis of SIRT7 in human lung cancer TMA. (A) The representative IHC images of Case 5 (tumor tissue IHC score: ‑), Case 37 (tumor tissue IHC score: +), Case 69 (tumor tissue IHC score: ++) and Case 6 (tumor tissue IHC score: +++). (B) The number of IHC scoring ‑, +, ++ or +++ cases in 102 paired lung cancer tumor/adjacent non‑tumor tissues. P<0.001, Mann‑Whitney U test. (C) The percentage of high/low SIRT7 expression in lung cancer tumor/adjacent non‑tumor tissues. *P<0.05, Pearson's χ2 test. T, tumor tissue; N, adjacent non‑tumor tissue. (D) The relative level of SIRT7 mRNA in human NSCLC cells (HBEpiC served as a control) analyzed by RT‑qPCR. (E and F) Analysis of SIRT7 protein in NSCLC cells by western blotting. (E) The representative western blot images. (F) The relative level of SIRT7 protein in NSCLC cells (HBEpiC served as a control). *P<0.05, one‑way repeated measures ANOVA with LSD post hoc multiple comparisons, n=6 per group. SIRT7, sirtuin 7; IHC, immunohistochemistry; TMS, tissue microarray; NSCLC, non‑small cell lung cancer; ANOVA, analysis of variance; LSD, least significant difference.

    Article Snippet: The pGEM/SIRT7 cloning plasmid carrying human SIRT7 coding sequence (CDS) (BC017305) was supplied by Sino Biological, Inc. Plasmids including pLenti6.3/IRES/GFP lentiviral plasmid-expressing blasticidin S deaminase and green fluorescent protein (GFP) as well as pLP1, pLP2 and VSVG lentiviral packing plasmids were supplied by Novobio Scientific, Inc. Lentiviruses including control shRNA lentivirus (LV-shcontrol) and SIRT7 shRNA (h) lentivirus (LV-shSIRT7) containing puromycin resistance gene were supplied by Santa Cruz Biotechnology, Inc.

    Techniques: Mann-Whitney U-Test, Expressing, Control, Western Blot, Immunohistochemistry, Microarray

    Figure 2. Overexpression/knockdown of SIRT7 in human NSCLC cells. (A) GFP analysis by fluorescence microscopy. (B) GFP analysis by flow cytometry. (C) SIRT7 overexpression or knockdown efficiency detected by RT‑qPCR. (D) SIRT7 overexpression or knockdown efficiency detected by western blotting. The representative western blot images are presented in the upper panel. The relative level of SIRT7 protein in A549‑SIRT7 (A549‑mock served as a control) and H292‑shSIRT7 (H292‑shcontrol served as a control) NSCLC cells are presented in the lower panel. *P<0.05, Student's t‑test, n=6 per group. SIRT7, sirtuin 7; NSCLC, non‑small cell lung cancer; GFP, green fluorescent protein; reverse transcription‑quantitative PCR.

    Journal: Oncology reports

    Article Title: Sirtuin 7 promotes non‑small cell lung cancer progression by facilitating G1/S phase and epithelial‑mesenchymal transition and activating AKT and ERK1/2 signaling.

    doi: 10.3892/or.2020.7672

    Figure Lengend Snippet: Figure 2. Overexpression/knockdown of SIRT7 in human NSCLC cells. (A) GFP analysis by fluorescence microscopy. (B) GFP analysis by flow cytometry. (C) SIRT7 overexpression or knockdown efficiency detected by RT‑qPCR. (D) SIRT7 overexpression or knockdown efficiency detected by western blotting. The representative western blot images are presented in the upper panel. The relative level of SIRT7 protein in A549‑SIRT7 (A549‑mock served as a control) and H292‑shSIRT7 (H292‑shcontrol served as a control) NSCLC cells are presented in the lower panel. *P<0.05, Student's t‑test, n=6 per group. SIRT7, sirtuin 7; NSCLC, non‑small cell lung cancer; GFP, green fluorescent protein; reverse transcription‑quantitative PCR.

    Article Snippet: The pGEM/SIRT7 cloning plasmid carrying human SIRT7 coding sequence (CDS) (BC017305) was supplied by Sino Biological, Inc. Plasmids including pLenti6.3/IRES/GFP lentiviral plasmid-expressing blasticidin S deaminase and green fluorescent protein (GFP) as well as pLP1, pLP2 and VSVG lentiviral packing plasmids were supplied by Novobio Scientific, Inc. Lentiviruses including control shRNA lentivirus (LV-shcontrol) and SIRT7 shRNA (h) lentivirus (LV-shSIRT7) containing puromycin resistance gene were supplied by Santa Cruz Biotechnology, Inc.

    Techniques: Over Expression, Knockdown, Fluorescence, Microscopy, Flow Cytometry, Western Blot, Control

    Figure 3. SIRT7 promotes growth and G1 to S‑phase transition of human NSCLC cells. (A) CCK‑8 analysis of NSCLC cell proliferation/growth. *P<0.05, two‑way repeated measures ANOVA with LSD post hoc multiple comparisons, n=6 per group. (B and C) Colony formation assay. (B) The representative images. (C) The relative clonogenic ability of A549‑SIRT7 (A549‑mock served as a control) and H292‑shSIRT7 (H292‑shcontrol served as a control) NSCLC cells. *P<0.05, Student t‑test, n=6 per group. (D‑F) Tumor subcutaneous xenograft mouse model. (D) Tumor volume. *P<0.05, two‑way repeated measures ANOVA with LSD post hoc multiple comparisons, n=6 per group. (E) The xenograft tumor images. (F) Tumor weight. *P<0.05, Student's t‑test, n=6 per group. (G and H) Cell cycle analysis by flow cytometry. (G) The representative images. (H) The percentage of each cell cycle phase. *P<0.05, Student's t‑test, n=6 per group. SIRT7, sirtuin 7; NSCLC, non‑small cell lung cancer; CCK‑8, Cell Counting Kit‑8; ANOVA, analysis of variance; LSD, least significant difference.

    Journal: Oncology reports

    Article Title: Sirtuin 7 promotes non‑small cell lung cancer progression by facilitating G1/S phase and epithelial‑mesenchymal transition and activating AKT and ERK1/2 signaling.

    doi: 10.3892/or.2020.7672

    Figure Lengend Snippet: Figure 3. SIRT7 promotes growth and G1 to S‑phase transition of human NSCLC cells. (A) CCK‑8 analysis of NSCLC cell proliferation/growth. *P<0.05, two‑way repeated measures ANOVA with LSD post hoc multiple comparisons, n=6 per group. (B and C) Colony formation assay. (B) The representative images. (C) The relative clonogenic ability of A549‑SIRT7 (A549‑mock served as a control) and H292‑shSIRT7 (H292‑shcontrol served as a control) NSCLC cells. *P<0.05, Student t‑test, n=6 per group. (D‑F) Tumor subcutaneous xenograft mouse model. (D) Tumor volume. *P<0.05, two‑way repeated measures ANOVA with LSD post hoc multiple comparisons, n=6 per group. (E) The xenograft tumor images. (F) Tumor weight. *P<0.05, Student's t‑test, n=6 per group. (G and H) Cell cycle analysis by flow cytometry. (G) The representative images. (H) The percentage of each cell cycle phase. *P<0.05, Student's t‑test, n=6 per group. SIRT7, sirtuin 7; NSCLC, non‑small cell lung cancer; CCK‑8, Cell Counting Kit‑8; ANOVA, analysis of variance; LSD, least significant difference.

    Article Snippet: The pGEM/SIRT7 cloning plasmid carrying human SIRT7 coding sequence (CDS) (BC017305) was supplied by Sino Biological, Inc. Plasmids including pLenti6.3/IRES/GFP lentiviral plasmid-expressing blasticidin S deaminase and green fluorescent protein (GFP) as well as pLP1, pLP2 and VSVG lentiviral packing plasmids were supplied by Novobio Scientific, Inc. Lentiviruses including control shRNA lentivirus (LV-shcontrol) and SIRT7 shRNA (h) lentivirus (LV-shSIRT7) containing puromycin resistance gene were supplied by Santa Cruz Biotechnology, Inc.

    Techniques: Colony Assay, Control, Cell Cycle Assay, Flow Cytometry, CCK-8 Assay

    Figure 4. SIRT7 facilitates human NSCLC cell in vitro migration and invasion as well as in vivo distant lung metastasis. (A and B) Wound healing assay. (A) The representative images. (B) The relative migratory ability of A549‑SIRT7 (A549‑mock served as a control) and H292‑shSIRT7 (H292‑shcontrol served as a control) NSCLC cells. (C and D) Transwell migration assay. (C) The representative images. (D) The relative migratory ability of the aforementioned cells. (E and F) Transwell invasion assay. (E) The representative images. (F) The relative invasive ability of the aforementioned cells. (G) The representative H&E staining images of lung tissues. (H) The number of tumor metastatic nodules in lung tissues. *P<0.05, Student's t‑test, n=6 per group. SIRT7, sirtuin 7; NSCLC, non‑small cell lung cancer; H&E, hematoxylin and eosin.

    Journal: Oncology reports

    Article Title: Sirtuin 7 promotes non‑small cell lung cancer progression by facilitating G1/S phase and epithelial‑mesenchymal transition and activating AKT and ERK1/2 signaling.

    doi: 10.3892/or.2020.7672

    Figure Lengend Snippet: Figure 4. SIRT7 facilitates human NSCLC cell in vitro migration and invasion as well as in vivo distant lung metastasis. (A and B) Wound healing assay. (A) The representative images. (B) The relative migratory ability of A549‑SIRT7 (A549‑mock served as a control) and H292‑shSIRT7 (H292‑shcontrol served as a control) NSCLC cells. (C and D) Transwell migration assay. (C) The representative images. (D) The relative migratory ability of the aforementioned cells. (E and F) Transwell invasion assay. (E) The representative images. (F) The relative invasive ability of the aforementioned cells. (G) The representative H&E staining images of lung tissues. (H) The number of tumor metastatic nodules in lung tissues. *P<0.05, Student's t‑test, n=6 per group. SIRT7, sirtuin 7; NSCLC, non‑small cell lung cancer; H&E, hematoxylin and eosin.

    Article Snippet: The pGEM/SIRT7 cloning plasmid carrying human SIRT7 coding sequence (CDS) (BC017305) was supplied by Sino Biological, Inc. Plasmids including pLenti6.3/IRES/GFP lentiviral plasmid-expressing blasticidin S deaminase and green fluorescent protein (GFP) as well as pLP1, pLP2 and VSVG lentiviral packing plasmids were supplied by Novobio Scientific, Inc. Lentiviruses including control shRNA lentivirus (LV-shcontrol) and SIRT7 shRNA (h) lentivirus (LV-shSIRT7) containing puromycin resistance gene were supplied by Santa Cruz Biotechnology, Inc.

    Techniques: In Vitro, Migration, In Vivo, Wound Healing Assay, Control, Transwell Migration Assay, Transwell Invasion Assay, Staining

    Figure 5. SIRT7 activates AKT/ERK1/2 signaling and regulates the expression of G1‑phase checkpoint molecules for G1 to S transition as well as EMT molecules for EMT induction in NSCLC cells. (A and B) Western blot analysis of AKT/ERK1/2, G1‑phase checkpoint and EMT molecules. (A) The represen- tative western blot images. (B) The relative level of p‑AKT (T308)/AKT, p‑AKT (S473)/AKT and p‑ERK1/2/ERK1/2 as well as p21, p27, cyclin D1, cyclin E1, CDK2, CDK4, E‑cadherin, N‑cadherin, vimentin, Snail and Slug in A549‑SIRT7 (A549‑mock served as a control) or H292‑shSIRT7 (H292‑shcontrol served as a control) NSCLC cells. *P<0.05, Student's t‑test, n=6 per group. (C) IHC analysis of AKT/ERK1/2, G1‑phase checkpoint and EMT molecules in xenograft tumor tissues. The representative IHC images are presented. SIRT7, sirtuin 7; EMT, epithelial‑mesenchymal transition; NSCLC, non‑small cell lung cancer; AKT, protein kinase; ERK1/2, extracellular signal‑regulated kinase 1/2; CDK, cyclin‑dependent kinase; IHC, immunohistochemistry.

    Journal: Oncology reports

    Article Title: Sirtuin 7 promotes non‑small cell lung cancer progression by facilitating G1/S phase and epithelial‑mesenchymal transition and activating AKT and ERK1/2 signaling.

    doi: 10.3892/or.2020.7672

    Figure Lengend Snippet: Figure 5. SIRT7 activates AKT/ERK1/2 signaling and regulates the expression of G1‑phase checkpoint molecules for G1 to S transition as well as EMT molecules for EMT induction in NSCLC cells. (A and B) Western blot analysis of AKT/ERK1/2, G1‑phase checkpoint and EMT molecules. (A) The represen- tative western blot images. (B) The relative level of p‑AKT (T308)/AKT, p‑AKT (S473)/AKT and p‑ERK1/2/ERK1/2 as well as p21, p27, cyclin D1, cyclin E1, CDK2, CDK4, E‑cadherin, N‑cadherin, vimentin, Snail and Slug in A549‑SIRT7 (A549‑mock served as a control) or H292‑shSIRT7 (H292‑shcontrol served as a control) NSCLC cells. *P<0.05, Student's t‑test, n=6 per group. (C) IHC analysis of AKT/ERK1/2, G1‑phase checkpoint and EMT molecules in xenograft tumor tissues. The representative IHC images are presented. SIRT7, sirtuin 7; EMT, epithelial‑mesenchymal transition; NSCLC, non‑small cell lung cancer; AKT, protein kinase; ERK1/2, extracellular signal‑regulated kinase 1/2; CDK, cyclin‑dependent kinase; IHC, immunohistochemistry.

    Article Snippet: The pGEM/SIRT7 cloning plasmid carrying human SIRT7 coding sequence (CDS) (BC017305) was supplied by Sino Biological, Inc. Plasmids including pLenti6.3/IRES/GFP lentiviral plasmid-expressing blasticidin S deaminase and green fluorescent protein (GFP) as well as pLP1, pLP2 and VSVG lentiviral packing plasmids were supplied by Novobio Scientific, Inc. Lentiviruses including control shRNA lentivirus (LV-shcontrol) and SIRT7 shRNA (h) lentivirus (LV-shSIRT7) containing puromycin resistance gene were supplied by Santa Cruz Biotechnology, Inc.

    Techniques: Expressing, Western Blot, Control, Immunohistochemistry

    Figure 6. SIRT7 promotes NSCLC cell proliferation and EMT progression by activating AKT signaling. (A) CCK‑8 assay after treatment with an AKT inhib- itor (MK‑2206). *P<0.05 compared with A549‑SIRT7 or A549‑SIRT7+DMSO, two‑way repeated measures ANOVA with LSD post hoc multiple comparisons, n=6 per group. (B) Wound healing assay after treatment with the AKT inhibitor (MK‑2206). *P<0.05 compared with A549‑SIRT7 or A549‑SIRT7+DMSO, one‑way repeated measures ANOVA with LSD post hoc multiple comparisons, n=6 per group. (C) Transwell invasion assay after treatment with the AKT inhibitor. *P<0.05 compared with A549‑SIRT7 or A549‑SIRT7+DMSO, one‑way repeated measures ANOVA with LSD post hoc multiple comparisons, n=6 per group. (D) Western blot analysis of EMT markers after treatment with the AKT inhibitor. The representative western blot images are presented. SIRT7, sirtuin 7; EMT, epithelial‑mesenchymal transition; NSCLC, non‑small cell lung cancer; EMT, epithelial‑mesenchymal transition; AKT, protein kinase B; CCK‑8, Cell Counting Kit‑8; DMSO, dimethylsulfoxide; ANOVA, analysis of variance; LSD, least significant difference.

    Journal: Oncology reports

    Article Title: Sirtuin 7 promotes non‑small cell lung cancer progression by facilitating G1/S phase and epithelial‑mesenchymal transition and activating AKT and ERK1/2 signaling.

    doi: 10.3892/or.2020.7672

    Figure Lengend Snippet: Figure 6. SIRT7 promotes NSCLC cell proliferation and EMT progression by activating AKT signaling. (A) CCK‑8 assay after treatment with an AKT inhib- itor (MK‑2206). *P<0.05 compared with A549‑SIRT7 or A549‑SIRT7+DMSO, two‑way repeated measures ANOVA with LSD post hoc multiple comparisons, n=6 per group. (B) Wound healing assay after treatment with the AKT inhibitor (MK‑2206). *P<0.05 compared with A549‑SIRT7 or A549‑SIRT7+DMSO, one‑way repeated measures ANOVA with LSD post hoc multiple comparisons, n=6 per group. (C) Transwell invasion assay after treatment with the AKT inhibitor. *P<0.05 compared with A549‑SIRT7 or A549‑SIRT7+DMSO, one‑way repeated measures ANOVA with LSD post hoc multiple comparisons, n=6 per group. (D) Western blot analysis of EMT markers after treatment with the AKT inhibitor. The representative western blot images are presented. SIRT7, sirtuin 7; EMT, epithelial‑mesenchymal transition; NSCLC, non‑small cell lung cancer; EMT, epithelial‑mesenchymal transition; AKT, protein kinase B; CCK‑8, Cell Counting Kit‑8; DMSO, dimethylsulfoxide; ANOVA, analysis of variance; LSD, least significant difference.

    Article Snippet: The pGEM/SIRT7 cloning plasmid carrying human SIRT7 coding sequence (CDS) (BC017305) was supplied by Sino Biological, Inc. Plasmids including pLenti6.3/IRES/GFP lentiviral plasmid-expressing blasticidin S deaminase and green fluorescent protein (GFP) as well as pLP1, pLP2 and VSVG lentiviral packing plasmids were supplied by Novobio Scientific, Inc. Lentiviruses including control shRNA lentivirus (LV-shcontrol) and SIRT7 shRNA (h) lentivirus (LV-shSIRT7) containing puromycin resistance gene were supplied by Santa Cruz Biotechnology, Inc.

    Techniques: CCK-8 Assay, Inhibition, Wound Healing Assay, Transwell Invasion Assay, Western Blot