Journal: Genes & Diseases

Article Title: Blockade of co-inhibitory receptor immune checkpoint protein TIM3/CD366 augments the anti-cancer activity of CAR-T therapy in solid tumors: An ovarian cancer example

doi: 10.1016/j.gendis.2025.101978

Figure Lengend Snippet: Specific IFN-γ and TNF-α release of T lymphocytes transduced with TIM-3-silenced HER2-specific chimeric antigen receptor (CAR) or HER2-specific CAR. (A, B) TIM-3-silenced CAR-T cells and control T cells were co-incubated with Galectin-9 + or Galectin-9 – SKOV3 tumor cells (E:T ratio 5:1 or 10:1). At 20 h after coculture, a specific enzyme-linked immunosorbent assay was used to analyze the supernatant for IFN-γ cytokine-release. Results were presented as mean ± standard deviation. (C, D) The detection of TNF-α in the same culture supernatant. Results were presented as mean ± standard deviation. ∗ P < 0.05 and ∗∗ P < 0.01.

Article Snippet: Human cervical cancer cell line HeLa, lentivirus packaging cell line HEK 293TD, and human ovarian cancer cell line SKOV3 were purchased from American Type Culture Collection (Manassas, Virginia, USA) and cultured in Dulbecco's modified Eagle's medium (Invitrogen, Grand Island, New York) supplemented with 10% heat-inactivated fetal bovine serum.

Techniques: Transduction, Control, Incubation, Enzyme-linked Immunosorbent Assay, Standard Deviation

Journal: Genes & Diseases

Article Title: Blockade of co-inhibitory receptor immune checkpoint protein TIM3/CD366 augments the anti-cancer activity of CAR-T therapy in solid tumors: An ovarian cancer example

doi: 10.1016/j.gendis.2025.101978

Figure Lengend Snippet: TIM-3 silencing augmented the anti-tumor activity of chimeric antigen receptor-T (CAR-T) cells in vivo . 2 × 10 6 SKOV3 tumor cells expressing luciferase were intraperitoneally inoculated in a xenograft mouse model, and 7 days after inoculation, the 2 × 10 6 HER2-specific CAR-T kdTim-3 cells or CAR-T cells, or untreated T cells were intraperitoneally administered. (A, B) Tumor growth was monitored using an in vivo imaging system. (C) Survival curve of 80-day post-treatment. ∗ P < 0.05 and ∗∗ P < 0.01.

Article Snippet: Human cervical cancer cell line HeLa, lentivirus packaging cell line HEK 293TD, and human ovarian cancer cell line SKOV3 were purchased from American Type Culture Collection (Manassas, Virginia, USA) and cultured in Dulbecco's modified Eagle's medium (Invitrogen, Grand Island, New York) supplemented with 10% heat-inactivated fetal bovine serum.

Techniques: Activity Assay, In Vivo, Expressing, Luciferase, In Vivo Imaging

Journal: bioRxiv

Article Title: Developing a Multimodal miR-15a Mimic to Overcome PARP Inhibitor Resistance in Epithelial Ovarian Cancer

doi: 10.64898/2026.04.20.719456

Figure Lengend Snippet: (A) Schematic representation of hsa-miR-15a and MTX-5-FU-Gem-miR-15a, showing incorporation of 5-fluorouracil and gemcitabine into the miR-15a backbone and conjugation of methotrexate (MTX) to the passenger strand. (B-E) Dose-response curves showing cell viability following treatment with MTX-5-FU-Gem-miR-15a, unmodified miR-15a, and olaparib in SK-OV-3 (B), OVCAR-3 (C), A2780 (D), and UWB1.289 (E) cells. Data represent mean ± SD from n = 4 biological replicates.

Article Snippet: Human epithelial ovarian cancer (EOC) cell lines SK-OV-3, OVCAR-3, A2780, and UWB1.289 were obtained from the American Type Culture Collection (ATCC) and MilliporeSigma.

Techniques: Conjugation Assay

Journal: bioRxiv

Article Title: Developing a Multimodal miR-15a Mimic to Overcome PARP Inhibitor Resistance in Epithelial Ovarian Cancer

doi: 10.64898/2026.04.20.719456

Figure Lengend Snippet: (A) Representative histograms of DNA content (PI staining) in only negative control and MTX-5-FU-Gem-miR-15a treatment showing cell cycle distribution in SK-OV-3, OVCAR-3, A2780, and UWB1.289 cells following treatment. (B) Quantification of cell cycle distribution after treatment shown as fold change in G2/S ratio relative to negative control across cell lines. (C) Representative Annexin V/PI flow cytometry plots showing apoptosis in indicated cell lines. (D) Quantification of apoptotic cells (early + late apoptosis) shown as fold change relative to control. (E) Western blot analysis showing expression of cleaved PARP, BCL-2, BAX, and BAK following treatment; β-actin serves as a loading control. Data represent mean ± SD from n = 3 biological replicates. Statistical significance between two groups was determined using two-tailed Student’s t test. ns, not significant; *p < 0.05; **p < 0.01; ***p < 0.001; ****p < 0.0001.

Article Snippet: Human epithelial ovarian cancer (EOC) cell lines SK-OV-3, OVCAR-3, A2780, and UWB1.289 were obtained from the American Type Culture Collection (ATCC) and MilliporeSigma.

Techniques: Staining, Negative Control, Flow Cytometry, Control, Western Blot, Expressing, Two Tailed Test

Journal: bioRxiv

Article Title: Developing a Multimodal miR-15a Mimic to Overcome PARP Inhibitor Resistance in Epithelial Ovarian Cancer

doi: 10.64898/2026.04.20.719456

Figure Lengend Snippet: (A, C, E) Western blot analysis of canonical miR-15a target proteins in ovarian cancer cells treated with negative control, miR-15a, MTX-5-FU-Gem-miR-15a, or 5-FU + gemcitabine. Panel A, SK-OV-3; panel C, OVCAR-3; panel E, UWB1.289. (B, D, F) Densitometric quantification of the corresponding western blots normalized to β-actin. Data represent mean ± SD from n = 3 biological replicates. Statistical significance between two groups was determined using two-tailed Student’s t test. ns, not significant; *p < 0.05; **p < 0.01; ***p < 0.001; ****p < 0.0001.

Article Snippet: Human epithelial ovarian cancer (EOC) cell lines SK-OV-3, OVCAR-3, A2780, and UWB1.289 were obtained from the American Type Culture Collection (ATCC) and MilliporeSigma.

Techniques: Western Blot, Negative Control, Two Tailed Test

Journal: bioRxiv

Article Title: Developing a Multimodal miR-15a Mimic to Overcome PARP Inhibitor Resistance in Epithelial Ovarian Cancer

doi: 10.64898/2026.04.20.719456

Figure Lengend Snippet: (A-C) Dose-response curves for MTX-5-FU-Gem-miR-15a and olaparib in olaparib-resistant OVCAR-3/OlaR (A), SK-OV-3/OlaR (B), and UWB1.289/OlaR (C) cells. (D) Representative cell cycle histograms (PI staining) and quantification of fold change in G2/S ratio in resistant cell lines. (E) Representative Annexin V/PI plots and quantification of total apoptotic cells (early + late apoptosis). (F-G) Dose-response analysis of cell viability in OVCAR-3 (F) and SK-OV-3 (G) spheroid cultures treated with increasing concentrations of MTX-5-FU-Gem-miR-15a or olaparib. (H) Western blot analysis of WEE1, CHK1, CCND1, and BCL-2 in OVCAR-3 spheroid cultures following treatment; β-actin serves as the loading control. Data represent mean ± SD from n = 3 biological replicates. Statistical significance between two groups was determined using two-tailed Student’s t test. *p < 0.05; **p < 0.01; ***p < 0.001; ****p < 0.0001.

Article Snippet: Human epithelial ovarian cancer (EOC) cell lines SK-OV-3, OVCAR-3, A2780, and UWB1.289 were obtained from the American Type Culture Collection (ATCC) and MilliporeSigma.

Techniques: Staining, Western Blot, Control, Two Tailed Test

Journal: bioRxiv

Article Title: Developing a Multimodal miR-15a Mimic to Overcome PARP Inhibitor Resistance in Epithelial Ovarian Cancer

doi: 10.64898/2026.04.20.719456

Figure Lengend Snippet: (A) Schematic of the in vivo experimental design and treatment schedule. (B) Representative bioluminescence images of parental SK-OV-3 xenografts at endpoint. (C) Tumor growth curves over time for vehicle- and MTX-5-FU-Gem-miR-15a-treated parental xenografts. (D) Kaplan-Meier survival analysis of parental xenografts. (E) Serum AST and ALT measurements evaluating treatment-associated toxicity. (F) Representative bioluminescence images of resistant SK-OV-3/OlaR xenografts treated with vehicle, intravenous MTX-5-FU-Gem-miR-15a, or intraperitoneal MTX-5-FU-Gem-miR-15a. (G) Tumor growth curves over time for resistant xenografts. (H) Proposed mechanistic model of MTX-5-FU-Gem-miR-15a activity. Data represent mean ± SD. Statistical significance for tumor growth and body weight analyses was determined using two-way ANOVA with appropriate post hoc testing. Survival differences were analyzed using the log-rank (Mantel-Cox) test. ns, not significant; *p < 0.05; **p < 0.01; ***p < 0.001; ****p < 0.0001.

Article Snippet: Human epithelial ovarian cancer (EOC) cell lines SK-OV-3, OVCAR-3, A2780, and UWB1.289 were obtained from the American Type Culture Collection (ATCC) and MilliporeSigma.

Techniques: In Vivo, Activity Assay

Journal: NPJ Precision Oncology

Article Title: GLUD1 supports ovarian cancer progression by counteracting anoikis via ARAF/MEK/ERK signaling

doi: 10.1038/s41698-026-01349-6

Figure Lengend Snippet: A Volcano plot of GLUD1 expression in epithelial ovarian cancer (EOC) from GEO datasets. Colors indicate gene expression levels: red for high, blue for low, and gray for non-significant expression changes. B Venn diagram illustrating the overlap among DEGs, anoikis-related genes, and amino acid metabolism–related genes. C GLUD1 expression in the GSE27651 dataset. Gene expression levels are shown with red representing tumor tissues and blue representing normal controls. D Kaplan-Meier curves showing overall survival differences between high and low GLUD1 expression groups in EOC patients from the TCGA dataset. Red and blue lines represent high and low expression levels, respectively. E Western blot analysis of GLUD1 expression in OVCAR3 and SKOV3 cells cultured under detached conditions. GAPDH was used as a loading control. F Representative immunohistochemistry images (Upper) and quantification (Lower) of GLUD1 expression in para-tumor, primary, and metastatic EOC tissues. G Overall survival curve and disease-free survival curve for EOC patients with low or high expression of GLUD1 based on IHC staining index. Data are presented as mean ± SD. * p < 0.05, ** p < 0.01.

Article Snippet: The human embryonic kidney cell line HEK293T and human ovarian cancer cell lines SKOV3, OVCAR3, HO8910PM, ES-2, A2780, and Caov-3 were obtained from the American Type Culture Collection (ATCC, Manassas, VA, USA).

Techniques: Expressing, Gene Expression, Western Blot, Cell Culture, Control, Immunohistochemistry

Journal: NPJ Precision Oncology

Article Title: GLUD1 supports ovarian cancer progression by counteracting anoikis via ARAF/MEK/ERK signaling

doi: 10.1038/s41698-026-01349-6

Figure Lengend Snippet: A Western blot analysis of GLUD1 expression in ovarian cancer cells with GLUD1 overexpression or knockdown. B Representative fluorescence images of live (green) and dead (red) cells under detached conditions (left) and quantification of live dead cell ratios (right). C Flow cytometric analysis of apoptosis in ovarian cancer cells cultured under detached conditions and corresponding quantification. D Transwell migration assays of SKOV3 and OVCAR3 cells with GLUD1 overexpression or knockdown and quantification of migrated cells. E Wound healing assays assessing migratory capacity of SKOV3 and OVCAR3 cells and quantification of wound closure. All experiments were performed in three independent biological replicates. Data are presented as mean ± SD. * p < 0.05, ** p < 0.01, *** p < 0.001.

Article Snippet: The human embryonic kidney cell line HEK293T and human ovarian cancer cell lines SKOV3, OVCAR3, HO8910PM, ES-2, A2780, and Caov-3 were obtained from the American Type Culture Collection (ATCC, Manassas, VA, USA).

Techniques: Western Blot, Expressing, Over Expression, Knockdown, Fluorescence, Cell Culture, Migration