The CCDC6 Knockout MES-OV Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout cell population designed to disrupt the tumor suppressor gene CCDC6 in a human ovarian carcinoma background. This loss-of-function model provides a genetically modified cell system for investigating the roles of CCDC6 in DNA damage response, apoptosis, and tumor suppression. The polyclonal format enables the study of heterogeneous knockout effects, bypassing clonal selection artifacts, and is suitable for functional genomics and pathway analysis.
The parental MES-OV cell line is an epithelial ovarian cancer cell line derived from an ovarian carcinoma, serving as a physiologically relevant model for ovarian cancer research. It retains key features of ovarian epithelial cells, making it a valuable tool for studying ovarian tumor biology, drug responses, and the molecular mechanisms underlying malignant transformation.
CCDC6 encodes a coiled-coil domain-containing protein that functions as a critical tumor suppressor in DNA damage signaling. It is activated by ATM and ATR kinases upon genotoxic stress, forming complexes with PP4 and interacting with CREB1 to modulate p53 stability and transcriptional activity. This regulation promotes expression of pro-apoptotic factor BAX, leading to apoptosis. Therefore, CCDC6 acts as a mediator that links DNA damage sensing to p53-dependent cell death, and its disruption compromises apoptotic signaling and DNA repair, thereby promoting genomic instability.
In the context of MES-OV ovarian carcinoma cells, knockout of CCDC6 disrupts the DNA damage-induced apoptotic pathway, potentially conferring resistance to DNA-damaging chemotherapeutics commonly used in ovarian cancer treatment. This model is thus instrumental for exploring tumor suppressor loss mechanisms, genomic instability, and drug resistance phenotypes specifically in ovarian cancer, a disease where CCDC6 may play a role in tumor progression and therapeutic response.
Typical research applications include mechanistic studies of DNA damage response using ??H2AX immunofluorescence and comet assay, apoptosis evaluation by caspase activation and cell viability assays, and drug sensitivity profiling to assess resistance to platinum-based agents or PARP inhibitors. Further analyses can involve western blotting and RT-qPCR for p53, BAX, and downstream targets. This cell population is also suitable for biomarker discovery and screening of compounds that restore apoptosis. For further technical details or ordering information, please contact Ascent Research.
