OVCAR-3
Cat.No.: CSC-C9120W
Species: Homo sapiens (Human)
Source: Ascites Metastasis
Morphology: epithelial
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Established in 1982 from the malignant ascites of a patient with progressive ovarian adenocarcinoma following combination chemotherapy, OVCAR-3 is one of the most extensively characterized and widely utilized cell lines in ovarian cancer research. Bioinformatic and molecular analyses have firmly established OVCAR-3 as a faithful representative model of high-grade serous ovarian carcinoma (HGSOC), exhibiting the defining genomic hallmarks of the disease: functional loss of TP53, low somatic mutation burden, and high copy-number alteration frequency closely mirroring TCGA HGSOC profiles.
OVCAR-3 uniquely bridges chemoresistance and chemosensitivity phenotypes. While originally derived from a tumor clinically refractory to cisplatin, doxorubicin, and cyclophosphamide, the line demonstrates marked sensitivity to carboplatin and the PARP inhibitor rucaparib—comparable to BRCA-mutant models—attributed to functional homologous recombination repair deficiency. Concurrently, it harbors high non-homologous end-joining activity and amplifications in DNA damage response genes including ATR and TOPBP1, offering a sophisticated platform for dissecting DDR pathway dependencies and synthetic lethalities.
Stemness and EMT Profiles Shift in Xenografts Derived from Cisplatin-Sensitive and Cisplatin-Tolerant Ovarian Cancer Cells
The transcriptional alterations underlying epithelial-to-mesenchymal transition (EMT) in chemoresistant ovarian cancer remain a matter of debate, with emerging evidence pointing to tumor cell plasticity and subclone reprogramming.
In this study, Mrkvicova, Alena, et al. developed a cisplatin-tolerant ovarian cancer model by treating the cisplatin-sensitive OVCAR-3 cell line with a single dose of cisplatin, generating the OVCAR-3 CP variant. These cisplatin-tolerant cells exhibited distinct EMT-related changes at both transcriptomic and protein levels, potentially regulated by epigenetic mechanisms. EMT profiling revealed that OVCAR-3 CP cells did not display a pronounced mesenchymal phenotype but rather retained epithelial characteristics and showed elevated expression of ALDH3A1. In contrast, the parental chemosensitive OVCAR-3 cells expressed canonical mesenchymal markers (CDH2, VIM, ZEB1/2, SNAIL, SLUG) and lacked stemness marker expression. Upon xenografting, both OVCAR-3 and OVCAR-3 CP cells demonstrated phenotypic plasticity, with parental OVCAR-3 xenografts acquiring EMT-like features resembling to those observed in cisplatin-tolerant tumors. These findings suggest a decoupling of EMT from cisplatin-tolerance and instead underscore a stronger association between stemness traits and cisplatin tolerance.
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