The CCDC97 Knockout MES-OV Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population with targeted disruption of the CCDC97 gene in the human MES-OV cell line. This loss-of-function model enables systematic studies of CCDC97 in DNA repair and genomic stability within an ovarian cancer background. The polyclonal nature avoids clonal artifacts and is ideal for population-based functional genomics and drug response profiling.
MES-OV is an epithelial cell line derived from human ovarian endometrioid adenocarcinoma, known for defects in homologous recombination and DNA damage response. It retains sensitivity to platinum-based drugs and crosslinking agents, making it relevant for studying DNA repair and therapy resistance. This line is widely used to investigate genomic instability and tumor progression in the context of the Fanconi anemia/BRCA network.
CCDC97 encodes a coiled-coil protein essential for Fanconi anemia interstrand crosslink repair. It directly interacts with FANCD2, promoting its stability, monoubiquitination, and chromatin localization at damage sites. Upstream, CCDC97 responds to DNA damaging agents like mitomycin C and cisplatin, and is regulated by ATR kinase and the FANCI-FANCD2 complex. Downstream, CCDC97 facilitates recruitment of repair factors including BRCA1, BRCA2, and FAAP20, functioning within the Fanconi anemia core complex to repair crosslinks and maintain genome stability.
In ovarian cancer, CCDC97 knockout cells allow dissection of the Fanconi anemia pathway??s role in chemotherapeutic response. Loss of CCDC97 impairs crosslink repair, likely modifying sensitivity to agents like cisplatin and inducing genomic instability??key features of ovarian cancer progression. This model helps elucidate how CCDC97 deficiency affects DNA damage signaling and FANCD2-dependent repair, contributing to pathology in endometrioid and other ovarian carcinomas with DNA repair defects.
Applications include mechanistic studies of DNA damage response, Fanconi anemia pathway analysis, and investigation of cisplatin resistance. The knockout cells are suited for Western blotting of FANCD2 and FANCD2-Ub, immunofluorescence of damage-induced foci, chromatin fractionation, cell survival assays with crosslinking agents, flow cytometric cell cycle analysis, and co-immunoprecipitation of CCDC97 with FANCD2. For further technical information, please contact Ascent Research.
