The CCDC50 Knockout MES-OV Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population in which the CCDC50 gene has been disrupted via targeted genome editing. This heterogeneous loss-of-function model is designed to investigate the consequences of CCDC50 ablation in an ovarian carcinoma background, retaining the genetic diversity of the edited pool for robust analysis of CCDC50-dependent phenotypes without clonal selection artifacts. It is an ideal tool for researchers studying NF-??B signaling, apoptosis regulation, and tumorigenesis in the context of ovarian cancer.
MES-OV is a human ovarian endometrioid carcinoma-derived cell line that serves as a model for ovarian surface epithelial cell transformation. These cells exhibit hallmarks of ovarian malignancy, including deregulated proliferation, survival signaling, and altered apoptotic thresholds. As a clinically relevant platform, MES-OV enables dissection of oncogenic mechanisms driven by NF-??B pathway activation and provides a pertinent system for evaluating therapeutic strategies targeting survival signaling in ovarian cancer.
CCDC50 functions as an adaptor protein that bridges the deubiquitinase TNFAIP3 (A20) to its substrate RIPK1, thereby facilitating K63-linked ubiquitin chain editing and promoting termination of NF-??B signaling. By recruiting A20 to RIPK1, CCDC50 enables deubiquitination events that limit IKK complex activation, restricting phosphorylation and nuclear translocation of NF-??B p65. Loss of CCDC50 disrupts this regulatory mechanism, impairing A20-mediated deubiquitination and leading to persistent NF-??B activation and transcriptional upregulation of anti-apoptotic genes such as Bcl-2 and cIAPs. This results in enhanced cell survival and inhibition of caspase-dependent apoptosis. Operating downstream of TNF-??, CCDC50 integrates inputs from the TNFAIP3/NF-??B axis and interacts with K63-linked ubiquitin chains, positioning it as a critical node in the ubiquitin-mediated control of inflammatory and apoptotic responses.
In MES-OV cells, NF-??B hyperactivation is a hallmark of ovarian cancer that promotes tumor progression, chemoresistance, and immune evasion. CCDC50 knockout mimics loss-of-function scenarios observed in tumors, revealing its tumor-suppressive role in restraining NF-??B. Constitutive NF-??B activation in these polyclonal knockout cells permits detailed investigation of how aberrant ubiquitin editing contributes to ovarian cancer cell survival and drug resistance, and facilitates screening for synthetic lethality or bypass compounds.
These CCDC50 knockout polyclonal cells are applicable to a broad range of experimental assays, including Western blotting for CCDC50 and phosphorylated NF-??B p65, NF-??B luciferase reporter assays, and Annexin V staining to measure apoptosis. Co-immunoprecipitation studies with TNFAIP3 and ubiquitin chain analysis can further elucidate the role of CCDC50 in deubiquitination processes. Functional assessments via cell viability, migration, and invasion assays allow characterization of NF-??B-dependent phenotypes, while xenograft tumor growth studies provide in vivo evaluation of tumorigenic potential. The cell population is also valuable for investigating drug resistance mechanisms, inflammatory signaling pathways, and molecular links to lymphoma. For additional information, please contact Ascent Research.
