ov90 cells  (ATCC)

Journal: Journal of Extracellular Vesicles

Article Title: DNA Copy Number Profiling in Extracellular Vesicles as Clinical Biomarkers of High‐Grade Serous Ovarian Carcinoma

doi: 10.1002/jev2.70308

Figure Lengend Snippet: EV‐DNA as companion biomarker for PARP inhibitor treatment. (a) IC50 values of Kuramochi, OV90, and COV362 cells for olaparib. Kuramochi cells were classified as sensitive, OV90 cells as intermediate, and COV362 cells as resistant. (b) CNV status for sEV‐DNA from Kuramochi (sensitive), OV90 (intermediate), and COV362 (resistant) cells. (c) PCA of CNV profiles for responders and nonresponders. (d) Hierarchical clustering and heatmap showing the CNV profiles of responders and nonresponders. The copy number values were normalized to those of normal ovarian tissue derived from FFPE samples, with normal copy number defined as 1. The color scale represents relative copy number values, where values greater than 1 are shown in red (copy number gain), whereas values less than 1 are shown in blue (copy number loss). (e) CV scores showing the predictive performance of the 30‐gene panel. (f) Heatmap for the top 5 genes of CV scores. (g–i) ROC curves and AUC values for the selected gene panels. (g) Top 5 genes ranked by CV score. (h) Combination of NOTCH3 and CSMD3 using LASSO analysis. (i) Combination of ARID1A, NOTCH3, CSMD3, ELP4, and BARD1 using LASSO analysis. The green area represents the 95% confidence interval (CI), and AUC values are shown with corresponding CIs. (j) Copy numbers of the top 5 genes of CV scores for sEV‐DNA in ascites from patients with HGSOC who received olaparib as maintenance therapy. (k) Predictive scores of LASSO2 and LASSO5 for patients with HGSOC who received olaparib as maintenance therapy. The respective prediction equations were LASSO2: 0.2133 × NOTCH3 + 0.1967 × CSMD3 + 0.7894 and LASSO5: 0.24758 × ARID1A + 1.60957 × NOTCH3 + 1.95855 × CSMD3 + 0.02955 × ELP4 + 0.11231 × BARD1 – 2.6119. When the value of the equation is >0, the patient's prognosis is considered good; when it is <0, the prognosis is considered poor.

Article Snippet: CAOV3, OVCAR3, and OV90 cells were purchased from the ATCC.

Techniques: Biomarker Discovery, Derivative Assay

Journal: bioRxiv

Article Title: Abolishing respiratory complex I decreases in vivo growth of high grade serous ovarian cancer cells and sensitizes to anti-angiogenic therapy

doi: 10.64898/2026.02.28.708681

Figure Lengend Snippet: (a) HIF1a western blot analysis in representative OV-90 +/+ and OV90 −/− xenografts (n=3 per group). Calreticulin was used as loading control. (b) Gene expression of HIF1 targets evaluated by qRT-PCR in OV-90 +/+ (n=5) and OV-90 −/− (n=6) xenografts. Data were log transformed prior to statistical analysis. (c) Masson’s trichrome staining of OV-90 +/+ and OV90 −/− xenografts, with respective quantification of the stroma (collagen areas stained in blue). Representative images are shown with black squares indicating the insets of the areas shown at higher magnification. (d) Immunofluorescent staining of endomucin (Endo) and Smooth Muscle Actin (SMA) in OV-90 +/+ and OV-90 −/− xenografts, with nuclei stained with DAPI, scale bar 200 µm. White squares indicate the insets of the areas shown at higher magnification. Representative images are shown, together with quantification of total (Endo + ) and pericyte negative (Endo + SMA − ) vessels. (e) Ultrasound images of OV-90 +/+ and OV-90 −/− xenografts. Incoming (red) and outcoming (blue) blood flows are shown. The graph indicates the percentage of the blood flow areas detected within each tumor (n=3 per group). One-tailed t-test was used to compare averages between the groups. (f) Immunofluorescent staining of F4/80 + macrophages (red) in OV-90 +/+ and OV-90 −/− xenografts. White squares indicate the insets of the areas shown at higher magnification. The arrows indicate F4/80 + cells. Nuclei are stained with DAPI (blue), scale bar = 20 µm. For all panels, data in graphs are represented as mean ± SEM and p-value is indicated.

Article Snippet: The human HGSOC cell line OV90 was purchased from ATCC® (Manassas, VA, USA #CRL-3585).

Techniques: Western Blot, Control, Gene Expression, Quantitative RT-PCR, Transformation Assay, Staining, One-tailed Test

Journal: Cell Death & Disease

Article Title: Splice-switching of the oncogenic BCS1L isoform suppresses ovarian cancer progression by disrupting mitochondrial function

doi: 10.1038/s41419-026-08495-6

Figure Lengend Snippet: A Venn diagram of 53 BCS1L -bound splicing factors from the BCS1L RNA pulldown-MS in A2780 cells and 24 genes regulating BCS1L splicing derived from the TCGA-OV datasets (Pearson’s R > 0.15, p < 0.001). B Volcano plots of differentially expressed BCS1L -bound splicing factors between the TCGA-OV ( n = 374) dataset and the normal tissue in GTEx-ovary ( n = 180) datasets. |Pearson R | > 0.1 and p -value > 0.05 were considered significant. Positive correlations are shown in red, and negative correlations are shown in blue. C Relative BCS1L-L/BCS1L-S transcript expression was measured by qPCR in A2780 cells transfected with siRNAs targeting YBX1 , PUF60 , HSPA8 , USP39 , HNRNPF , SF3B4 , SNRPC , and SNRNP40 or a negative control for 48 h. D Sashimi plots of the alternative splicing pattern and USP39 direct binding sites in BCS1L were created with IGV using RNA-seq and RIP-seq data in A2780 cells. The light blue region indicates the alternative exon and the USP39-binding sites. E Semi-quantitative RT-PCR was performed to validate alternative splicing events in A2780 cells with USP39 knockdown using isoform-specific primers. F The relative expression ratio of BCS1L-L/BCS1L-S was analyzed in A2780 cells with USP39 depletion using isoform-specific primers. G Schematic diagram of the BCS1L minigene structure and alternative splicing products. H The expression of BCS1L minigene transcripts in 293T cells with USP39 depletion using different USP39 siRNAs as measured by semi-quantitative RT-PCR. I The expression of BCS1L minigene transcripts in 293T cells transfected with USP39 expression plasmids was measured by semi-quantitative RT-PCR. J The interaction between USP39 and BCS1L RNA was validated by RIP-qPCR of A2780 cells overexpressing USP39. U6snRNA served as the positive control. n = 3 biologically independent experiments. K RNA pull-down assay showing the interaction between the BCS1L RNA and USP39 protein in A2780 cells. Androgen receptor 3´-UTR RNA was used as the positive control and poly (A) 25 RNA was used as the negative control. L The protein expression of BCS1L-L and BCS1L-S was determined by western blot in A2780, HEY, and OV90 cells with USP39 knockdown and in OVCAR3 cells with USP39 overexpression. The top band at 48 kDa indicates BCS1L-L, and the bottom band at 34 kDa indicates BCS1L-S. M Representative confocal images of control A2780 cells and A2780 cells with USP39 knockdown showing co-localization of BCS1L (green) and COX4 (red). DAPI was used to visualize nuclei. Scale bars, 10 µm. Images are representative of at least three independent experiments. Co-localization coefficients, including Pearson correlation coefficient and Mander’s coefficient were quantified by Image J ( n = 50 cells for control, n = 50 cells for USP39 knockdown). The p -value ( C , F , J , M ) was obtained by Student’s unpaired t -test and and the results are presented as the mean ± SD. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001.

Article Snippet: Human ovarian cancer cell lines OV90, SKOV3, OVCAR3, OVCAR8, and CAOV3 were purchased from the American Type Culture Collection.

Techniques: Derivative Assay, Expressing, Transfection, Negative Control, Alternative Splicing, Binding Assay, RNA Sequencing, Quantitative RT-PCR, Knockdown, Positive Control, Pull Down Assay, Western Blot, Over Expression, Control

Journal: bioRxiv

Article Title: Cancer-Associated Mesothelial Cells Drive Immune Escape and Therapy Resistance in Ovarian Cancer

doi: 10.64898/2026.01.07.698232

Figure Lengend Snippet: A) Quantitative PCR (qPCR) analysis of Upk3b and Serpinb2 expression in immortalized mesothelial cells (iMC) stimulated with KPCA-conditioned media and Met5a stimulated with patient D HGSOC media (ptD) or Ov90 ovarian cancer cell line in a time-dependent manner (0-96hrs). B) Western blot analysis of UPK3B and SERPINB2 expression in iMC treated with KPCA-condioned culture medium at 0h, 24h, 48h, 72h and 96h (left panel) and Met5A stimulated with conditioned media from ptD/Ov90 cell-lines versus unstimulated controls at 72h (right panel). C) Immunofluorescence analysis of UPK3B and SERPINB2 in iMC and Met5A comparing conditions stimulated with either KPCA-conditioned media or ptD/Ov90 media versus unstimulated controls at 72 h. D) Immunofluorescence staining for ACTA2 and COL4A1 in both primary MCs and immortalized MCs (iMCs) after 96 hours of exposure to KPCA-conditioned media

Article Snippet: The KPCA cell lines were developed and described in Iyer et al. and the OV90 cells lines of malignant papillary serous adenocarcinoma were purchased from ATCC.

Techniques: Real-time Polymerase Chain Reaction, Expressing, Western Blot, Immunofluorescence, Staining