Journal: Frontiers in Immunology

Article Title: Multi-omics analysis and experiments uncover the link between cancer intrinsic drivers, stemness, and immunotherapy in ovarian cancer with validation in a pan-cancer census

doi: 10.3389/fimmu.2025.1549656

Figure Lengend Snippet: Cancer intrinsic drivers and stemness properties to portrait the path of OV progression. (A) tSNE plot showing the composition of 5 main subtypes derived from OV malignant cells. (B) Heatmap showing expression programs derived in a representative patient using NMF. (C) Relative expression scores of meta-programs in each OV malignant cell cluster. (D) KEGG enrichment of cancer intrinsic driver and stemness associated mRNAs. (E) Venn diagram showing the overlap between intratumoral heterogeneity driven genes and cancer stemness associated genes. (F) AUCell score of selected 4 intrinsic variation driven cancer stemness associated genes in different cell types. (G) t-SNE visualizes the evolutionary trajectory of tumor cells calculated by slightshot. (H) Violin plots illustrating the expression of RAD21 and CSE1L across different malignant cell subtypes. (I) The relationship between gene expression and evolutionary time. (J) The correlation between inhibitory and RAD21, CSE1L in fifteen OV datasets.

Article Snippet: The primary antibodies used in this analysis included CSE1L (22219-1-AP, Proteintech, Wuhan, China) and Alpha Tubulin (11224-1-AP, Proteintech, Wuhan, China).

Techniques: Derivative Assay, Expressing, Gene Expression

Journal: Frontiers in Immunology

Article Title: Multi-omics analysis and experiments uncover the link between cancer intrinsic drivers, stemness, and immunotherapy in ovarian cancer with validation in a pan-cancer census

doi: 10.3389/fimmu.2025.1549656

Figure Lengend Snippet: Investigating CSE1L-related immune landscapes and providing drug therapy strategies. (A) Kaplan-Meier estimates of overall survival of patients in OV dataset ( GSE9891 ). (B) Box plots comparing the proportion of immune cells between low- and high- CSE1L groups ( GSE26712 ). (C) Heatmap of the expression of chemokines and their corresponding receptors, interferons and their corresponding receptors, and interleukins and their receptors in low- and high-CSE1L groups ( GSE26712 ). (D) Heatmap of the GSVA score of seven steps in cancer immunity cycle in low- and high- CSE1L groups ( GSE26712 ). (E) Heatmap of the expression of effector markers of tumor-infiltrating immune cells in low- and high-CSE1L groups ( GSE26712 ). (F) Box plots comparing the activity of JAK/STAT and VEGF pathway between low- and high- CSE1L groups ( GSE26712 ). (G) Dot plot showing the drug drug susceptibility of chemotherapy drugs. The x-axis represents the log2FC of IC50, where a positive value indicates that the IC50 of the low CSE1L group is greater than that of the high CSE1L group. The y-axis represents -log2 P-value ( GSE26712 ). The drugs highlighted in red are chemotherapy drugs that inhibit VEGF. (H) Box plots comparing the expression of CSE1L between low- and high- Stage groups in GSE30161 and GSE9891 . (I) Box plots comparing the expression of CSE1L between low- and high- Grade groups in GSE9891 . (Wilcoxon test; ns, no significant; *P < 0.05; ***P < 0.001).

Article Snippet: The primary antibodies used in this analysis included CSE1L (22219-1-AP, Proteintech, Wuhan, China) and Alpha Tubulin (11224-1-AP, Proteintech, Wuhan, China).

Techniques: Expressing, Activity Assay

Journal: Frontiers in Immunology

Article Title: Multi-omics analysis and experiments uncover the link between cancer intrinsic drivers, stemness, and immunotherapy in ovarian cancer with validation in a pan-cancer census

doi: 10.3389/fimmu.2025.1549656

Figure Lengend Snippet: CSE1L promotes progression of ovarian cancer in vitro . (A) Representative immunohistochemistry results showed that CSE1L expression was significantly upregulated in tumor tissues compared to adjacent non-cancerous tissues. (B) Validation of CSE1L of knockout in OVCAR-3 and A2780 cell lines by Western Blotting analysis. (C) Proliferation ability of CSE1L-knockout ovarian cancer cells detected by CCK8 assay. (D, E) Evaluation and quantitative analysis of the migration ability of CSE1L-knockout OVCAR-3 and A2780 cell lines using wound healing assays. (F) Analysis and quantitative assessment of the effect of CSE1L knockdown on the migration ability of ovarian cancer cells using Transwell assays. Scale bar, 100μm. (Wilcoxon test; *P < 0.05).

Article Snippet: The primary antibodies used in this analysis included CSE1L (22219-1-AP, Proteintech, Wuhan, China) and Alpha Tubulin (11224-1-AP, Proteintech, Wuhan, China).

Techniques: In Vitro, Immunohistochemistry, Expressing, Biomarker Discovery, Knock-Out, Western Blot, CCK-8 Assay, Migration, Knockdown

Journal: bioRxiv

Article Title: Regulation of lipid dysmetabolism and neuroinflammation linked with Alzheimer’s disease through modulation of Dgat2

doi: 10.1101/2025.02.18.638929

Figure Lengend Snippet: a, Flow chart depicting the experimental setup. Each UAS gene was crossed with the region-specific Gal-4 drivers. To explore the contribution of Dgat2 in Aβ42 and App accumulation, we performed Elav-driven Dgat2 KD and Dgat2 OE in Drosophila and used an App NLG-F mouse model with Dgat2 inhibitor . b, Negative geotaxis assay of Elav and GLaz drove A pp NLG and Aβ42 models in 3wk males and females . c-e, Memory assay of Drosophila : Original method, the difference between fly decisions, flies avoiding shock odor in Elav, GLaz and OK107 App NLG and Aβ42 models. Two-way ANOVA with multiple comparisons done with Uncorrected Fisher’s LSD test was performed for geotaxis, n=3 replicates per group and each group had 10 flies. Chi-square tests were performed for memory assay, ( App NLG N=50, Aβ42=46, W 1118 =54, GFP=45 ). *P<0.05, **P<0.01 and ***P<0.001 n.s = not significant. Exact p values are provided in the source data.

Article Snippet: To investigate whether Dgat2 contributes to AD-related phenotypes, we used PF-06424439, a Dgat2 noncompetitive (MedChemExpress, CAS No#1469284-78-3), slowly reversible inhibitor with an IC50 of 14nM.

Techniques:

Journal: bioRxiv

Article Title: Regulation of lipid dysmetabolism and neuroinflammation linked with Alzheimer’s disease through modulation of Dgat2

doi: 10.1101/2025.02.18.638929

Figure Lengend Snippet: a, Negative geotaxis assay of Elav driven Dgat2 KD and OE in AD models in 3wk male and female . b-c, Memory assay of Drosophila: original method, difference between fly decisions, flies avoiding shock odor in Elav driven Dgat2 KD and OE in App NLG and Aβ42 . d-e, Total, day and night sleep (in minutes) and sleep fragmentation in Elav driven Dgat KD and OE in APP/aβ Models. Two-way ANOVA with multiple comparisons done with Uncorrected Fisher’s LSD test was performed for geotaxis, n=3 replicates per group and each group had 10 flies. Chi-square tests were performed for memory assay, (App NLG N=50, Aβ42=46, W 1118 =54, GFP=45). Non-parametric One-way ANOVA with multiple comparisons done with Kruskal Wallis test was performed for sleep activity and sleep fragmentation. Each dot represents several flies *P<0.05, **P<0.01 and ***P<0.001 n.s = not significant. Exact p values are provided in the source data.

Article Snippet: To investigate whether Dgat2 contributes to AD-related phenotypes, we used PF-06424439, a Dgat2 noncompetitive (MedChemExpress, CAS No#1469284-78-3), slowly reversible inhibitor with an IC50 of 14nM.

Techniques: Activity Assay

Journal: bioRxiv

Article Title: Regulation of lipid dysmetabolism and neuroinflammation linked with Alzheimer’s disease through modulation of Dgat2

doi: 10.1101/2025.02.18.638929

Figure Lengend Snippet: a, Representative image showing the expression of lipid accumulation (green), synaptic loss (purple), a marker of neurodegeneration, and DAPI (white) in the brains of Elav-driven KD in AD models in flies . b-c, Quantification of the expression level of lipid counts and synapsin intensity in Elav-driven AD models. d, Relative expression of inflammatory genes. e, Relative expression of metabolic genes in flies. f, Immunofluorescence staining showing the expression level of lipid spots and Gfap in hippocampus region of the brain of WT and App NLG-F mouse model in presence of Dgat2 inhibitor. g, Quantification of the Lipid spot expression level, h, Quantification of the Gfap expression level n=3 mice per group. i, Relative expression level of inflammatory and AD risk genes WT and App knock-in mouse models in the presence of Dgat2 inhibitor. One-way ANOVA with Turkey’s multiple comparisons test was performed for Flies data. N=3 replicates per group and each group has 8-10 flies. Two-way ANOVA with multiple comparisons done with Uncorrected Fisher’s LSD test was performed. *p < .05; **p < .01; ***p < .001; ns = not significant. Exact p values are provided in the source data.

Article Snippet: To investigate whether Dgat2 contributes to AD-related phenotypes, we used PF-06424439, a Dgat2 noncompetitive (MedChemExpress, CAS No#1469284-78-3), slowly reversible inhibitor with an IC50 of 14nM.

Techniques: Expressing, Marker, Immunofluorescence, Staining, Knock-In

Journal: bioRxiv

Article Title: Regulation of lipid dysmetabolism and neuroinflammation linked with Alzheimer’s disease through modulation of Dgat2

doi: 10.1101/2025.02.18.638929

Figure Lengend Snippet: a Relative Dgat2 transcription factors expressions level in Elav-driven App NLG and Aβ42 . b, Total, day and night sleep (minutes) and sleep fragmentation in Elav-driven Dgat2 TFs KD models. c, Representative image showing the expression of lipid accumulation (green), synaptic loss (purple), a marker of neurodegeneration, and DAPI (white) in the brains of Elav-driven Dgat2 TFs KD models . d-e, Quantification of the expression level of lipid counts and synapsin intensity in Elav-driven Dgat2 TFs KD models . f, Relative expressions level of AD risk genes in Elav driven Dgat2 TFs KD models. g-h, Relative expressions level of Dgat2 TFs and AD risk genes in App knock-in mouse model in presence of Dgat2 inhibitors. One-way ANOVA with Turkey’s multiple comparisons test was performed for Flies data. N=3 replicates per group and each group has 8-10 flies. n=3 mice per group. Two-way ANOVA with multiple comparisons done with Uncorrected Fisher’s LSD test was performed in mouse data. *p < .05; **p < .01; ***p < .001; ns = not significant. Exact p values are provided in the source data.

Article Snippet: To investigate whether Dgat2 contributes to AD-related phenotypes, we used PF-06424439, a Dgat2 noncompetitive (MedChemExpress, CAS No#1469284-78-3), slowly reversible inhibitor with an IC50 of 14nM.

Techniques: Expressing, Marker, Knock-In

Journal: bioRxiv

Article Title: Regulation of lipid dysmetabolism and neuroinflammation linked with Alzheimer’s disease through modulation of Dgat2

doi: 10.1101/2025.02.18.638929

Figure Lengend Snippet: Graphical illustration showed the impacts of panneuronal and glial specific expression of App NLG and Aβ42 without and with Dgat2 KD in Drosophila and microglial/ astrocytic activation and lipid accumulation in App NLG-F mouse model. The top panel result shows that panneuronal and glial-specific expression of App NLG and Aβ42 led to compromised locomotor and cognitive performance. It also led to enhanced lipid accumulation and reduced synapsin level, which were further rescued with Dgat2 KD (up and down arrows). The bottom panel shows the changes in Gfap, Ib1, Dgat2 stain, and Adrp protein in young/old and with Dgat2 inhibitors in APP NLG-F mouse model.

Article Snippet: To investigate whether Dgat2 contributes to AD-related phenotypes, we used PF-06424439, a Dgat2 noncompetitive (MedChemExpress, CAS No#1469284-78-3), slowly reversible inhibitor with an IC50 of 14nM.

Techniques: Expressing, Activation Assay, Staining

Journal: Technology and Health Care

Article Title: H 2 S improves doxorubicin-induced myocardial fibrosis by inhibiting oxidative stress and apoptosis via Keap1-Nrf2

doi: 10.3233/THC-218020

Figure Lengend Snippet: Expression of TNF- α , TGF- β 1, IL1 β , IL6, Bcl-2, caspase-3, caspase-9, Bax protein in myocardial tissue of each group. P * < 0.05 vs Control group; P # < 0.05 vs DOX group.

Article Snippet: Doxorubicin hydrochloride was purchased from Meilun Biotech Co., Ltd., China; TGF- β (BA0290), CSE (A04496), MMP8 (BM4427), MMP16 (A05065), TIMP1 (A00561), Collagen III (A00788), and primary antibody, anti-rabbit secondary antibody were purchased from Boster Company, China; TNF- α (17590-1-AP), Keap1 (10503-2-AP), caspase-3 (19677-1-AP), Caspase-9 (10380-1-AP), Bax (50599-2-Ig), IL1 β (16806-1-AP), IL6 (21865-1-AP), COX2 (66351-1-Ig), Nrf2 (16396-1-AP), NQO1 (11451-1-AP), HO-1 (10701-1-AP), GCLC (12601-1-AP) and Bcl-2 (12789-1-AP) were purchased from Proteintech; These antibodies are diluted 1:1000.

Techniques: Expressing, Control

Journal: PLoS ONE

Article Title: CASP8 SNP D302H (rs1045485) Is Associated with Worse Survival in MYCN -Amplified Neuroblastoma Patients

doi: 10.1371/journal.pone.0114696

Figure Lengend Snippet: 21 SNPs in 15 p53 pathway genes.

Article Snippet: CSE1L , rs2426127 , Intronic C>T , , , C__16230087_10 , 0.288.

Techniques:

Journal: Oncotarget

Article Title: MiR-542-5p is a negative prognostic factor and promotes osteosarcoma tumorigenesis by targeting HUWE1

doi:

Figure Lengend Snippet: A. Flow chart of proteomic analysis. B. Total identified and quantified proteins. All proteins had an unused protein score >1.3 and peptides ≥2. C. Heat map of upregulated and downregulated proteins in both MNNG/HOS and U2OS cells after transfection with miR-542-5p. D. E. Representative western blots displaying the levels of HUWE1, CSE1L and PTBP1 proteins after transfection with miR-542-5p mimics or inhibitors. β-actin was used as an internal control. F. The sequences of the putative miR-542-5p binding sites in wild type (emphasized with shadow) and mutant (red) HUWE1-3′UTR. G. The relative luciferase activity of luciferase reports with wild type or mutant HUWE1-3′UTR were determined in HEK 293T cells, which were co-transfected with the miR-542-5p mimic or miR-NC. Renilla luciferase activity served as an internal control. Statistical significance was observed between the wild type and the mutant groups transfected with miR-542-5p. The data are representative of three independent experiments. Error bars represent SEM. * P < 0.05 by Student's t test.

Article Snippet: After blocking in phosphate-buffered saline/Tween-20 containing 5% non-fat milk, the membranes were incubated with the following primary antibodies: HUWE1 (Bioworld Technology, 1:500), CSE1L (Bioworld Technology, USA, 1:500), PTBP1 (Bioworld Technology, 1:500) or β-actin (Sigma-Aldrich, 1:20000).

Techniques: Transfection, Western Blot, Binding Assay, Mutagenesis, Luciferase, Activity Assay

Journal: Aging (Albany NY)

Article Title: LncRNA BANCR promotes tumorigenesis and enhances adriamycin resistance in colorectal cancer

doi: 10.18632/aging.101530

Figure Lengend Snippet: BANCR and CSE1L were highly expressed in CRC tumor tissues. ( A and B ) Expressions of BANCR and CSE1L in 32 pairs of CRC tumor tissues and adjacent normal tissues. ( C ) Correlation analyses of BANCR and CSE1L expressions in CRC tumor tissues (n=21). * P < 0.05.

Article Snippet: Small interference RNAs (siRNAs) targeting BANCR (si-BANCR) and CSE1L (si-CSE1L), scramble control siRNA (si-Control), miR-203 mimic and its scramble control (miR-Control) were obtained from GenePharma Co. ltd (Suzhou, China).

Techniques:

Journal: Aging (Albany NY)

Article Title: LncRNA BANCR promotes tumorigenesis and enhances adriamycin resistance in colorectal cancer

doi: 10.18632/aging.101530

Figure Lengend Snippet: BANCR knockdown suppressed invasion, proliferation, induced apoptosis and increased ADR sensitivity in CRC cells. ( A ) Expression of BANCR in human normal colon mucosal epithelial cell line (NCM460) and CRC cell lines (LoVo and HCT116) was detected using RT-qPCR assay. (B-K) LoVo and HCT116 cells were transfected with si-Control or si-BANCR with untransfected (NC) or si-Control-transfected cells acted as blank or mock control, respectively. ( B and C ) Knockdown efficiency of si-BANCR was evaluated by RT-qPCR assays at 48 h upon transfection. ( D and E ) The effect of BANCR depletion on proliferation ability was measured by MTT assay at the indicated time points (0, 24, 48, 72 h) upon transfection in LoVo and HCT116 cells. ( F and G ) The effect of BANCR knockdown on invasion capability was assessed at 48 h after transfection by transwell invasion assay in LoVo and HCT116 cells. ( H and I ) The effect of BANCR deficiency on apoptotic rate was detected in LoVo and HCT116 cells at 48 h posttransfection by flow cytometry via double-staining of Annexin-V-FITC and PI. ( J and K ) LoVo and HCT116 cells were treated with different concentrations of ADR (0, 20, 40, 80, 160, 320, 640, 1280 ng/ml) for 48 h, followed by the determination of cell survival rate using MTT assay. * P < 0.05.

Article Snippet: Small interference RNAs (siRNAs) targeting BANCR (si-BANCR) and CSE1L (si-CSE1L), scramble control siRNA (si-Control), miR-203 mimic and its scramble control (miR-Control) were obtained from GenePharma Co. ltd (Suzhou, China).

Techniques: Knockdown, Expressing, Quantitative RT-PCR, Transfection, Control, MTT Assay, Transwell Invasion Assay, Flow Cytometry, Double Staining

Journal: Aging (Albany NY)

Article Title: LncRNA BANCR promotes tumorigenesis and enhances adriamycin resistance in colorectal cancer

doi: 10.18632/aging.101530

Figure Lengend Snippet: CSE1L overexpression abrogated si-BANCR-mediated anti-invasion, anti-proliferation and pro-apoptosis effects in CRC cells. ( A and B ) The effect of BANCR overexpression on CSE1 L protein level was detected in LoVo and HCT116 cells. ( C and D ) The effect of BANCR knockdown on CSE1 L protein expression was measured in LoVo and HCT116 cells. ( E - J ) LoVo and HCT116 cells were transfected with si-Control, si-BANCR, si-BANCR+pcDNA-Control, si-BANCR+pcDNA-CSE1L, followed by the determination of cell viability ( E and F ), invasion capacity ( G and H ) and apoptosis rate (I and J). * P < 0.05.

Article Snippet: Small interference RNAs (siRNAs) targeting BANCR (si-BANCR) and CSE1L (si-CSE1L), scramble control siRNA (si-Control), miR-203 mimic and its scramble control (miR-Control) were obtained from GenePharma Co. ltd (Suzhou, China).

Techniques: Over Expression, Knockdown, Expressing, Transfection, Control

Journal: Aging (Albany NY)

Article Title: LncRNA BANCR promotes tumorigenesis and enhances adriamycin resistance in colorectal cancer

doi: 10.18632/aging.101530

Figure Lengend Snippet: BANCR acted as a molecular sponge of miR-203 to sequester miR-203 away from CSE1L in CRC cells. ( A ) Predicted binding sites between BANCR and miR-203, and mutant sites in Mu-BANCR reporter. ( B and C ) The effects of miR-203 overexpression on luciferase activity of WT-BANCR and Mu-BANCR reporters were detected in LoVo and HCT116 cells. ( D ) Putative binding sequences between miR-203 and CSE1L 3’UTR, and mutant sites in CSE1L 3’UTR-Mu reporter. ( E and F ) The effects of miR-203 overexpression on luciferase activity of CSE1L 3’UTR-WT and CSE1L 3’UTR-Mu reporters were determination in LoVo and HCT116 cells.

Article Snippet: Small interference RNAs (siRNAs) targeting BANCR (si-BANCR) and CSE1L (si-CSE1L), scramble control siRNA (si-Control), miR-203 mimic and its scramble control (miR-Control) were obtained from GenePharma Co. ltd (Suzhou, China).

Techniques: Binding Assay, Mutagenesis, Over Expression, Luciferase, Activity Assay

Journal: Aging (Albany NY)

Article Title: LncRNA BANCR promotes tumorigenesis and enhances adriamycin resistance in colorectal cancer

doi: 10.18632/aging.101530

Figure Lengend Snippet: BANCR acted as a molecular sponge of miR-203 to sequester miR-203 away from CSE1L in CRC cells. ( G and H ) The effects of BANCR knockdown and overexpression on miR-203 expression were assessed in LoVo and HCT116 cells. ( I and J ) LoVo and HCT116 cells were transfected with miR-Control, miR-203, miR-203+pcDNA-Control, or miR-203+pcDNA-BANCR, followed by the measurement of CSE1L protein level. ( K ) miR-203 expression in 32 paired CRC tumor tissues and adjacent non-cancerous tissues. ( L and M ) Correlation analysis between miR-203 and BANCR or CSE1L in 32 paired CRC tumor tissues. ( N ) The effects of CSE1L silencing on 53BP1 and FEN1 expressions were tested in HCT116 cells. * P < 0.05.

Article Snippet: Small interference RNAs (siRNAs) targeting BANCR (si-BANCR) and CSE1L (si-CSE1L), scramble control siRNA (si-Control), miR-203 mimic and its scramble control (miR-Control) were obtained from GenePharma Co. ltd (Suzhou, China).

Techniques: Knockdown, Over Expression, Expressing, Transfection, Control

Journal: Aging (Albany NY)

Article Title: LncRNA BANCR promotes tumorigenesis and enhances adriamycin resistance in colorectal cancer

doi: 10.18632/aging.101530

Figure Lengend Snippet: BANCR knockdown inhibited tumor growth and enhanced ADR sensitivity by modulation of miR-203/ CSE1L pathway in vivo . LoVo/DOX cells stably infected lenti-sh-XIST or lenti-sh-Control were subcutaneously inoculated into, followed by injection with the left flank of mice, ADR (1 mg/kg) every 3 days on day 6 after cell inoculation. ( A ) Tumor volume was determined at the indicated time points (6, 9, 12, 15, 18, 21 days) after first injection. ( B ) At 21 days upon cell implantation, tumors were excised, imaged and weighted. ( C - E ) Expressions of BANCR, miR-203 and CSE1L in xenograft tumors were determined by RT-qPCR and western blot assays. * P < 0.05.

Article Snippet: Small interference RNAs (siRNAs) targeting BANCR (si-BANCR) and CSE1L (si-CSE1L), scramble control siRNA (si-Control), miR-203 mimic and its scramble control (miR-Control) were obtained from GenePharma Co. ltd (Suzhou, China).

Techniques: Knockdown, In Vivo, Stable Transfection, Infection, Control, Injection, Quantitative RT-PCR, Western Blot