The CCDC167 Knockout A2780 Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout cell population, specifically designed to disrupt the CCDC167 gene in the human A2780 ovarian carcinoma epithelial cell line. This gene-edited model provides a loss-of-function system to investigate the tumor suppressive roles of CCDC167, a protein implicated in the regulation of cell proliferation and apoptosis. The polyclonal population comprises a heterogeneous pool of edited cells, offering a robust and efficient means to study gene function without clonal isolation. Researchers can utilize this knockout model to explore downstream signaling events and cellular phenotypes associated with CCDC167 deficiency.
The host cell line A2780 is a well-characterized human ovarian carcinoma epithelial cell model derived from an endometrioid adenocarcinoma. Widely employed in oncology research, A2780 cells retain sensitivity to cisplatin, making them a valuable tool for studying drug response mechanisms in ovarian cancer. Their epithelial origin and tumorigenic properties render them particularly suitable for investigating cancer cell proliferation, apoptosis, and chemoresistance pathways. The genetic background of A2780 provides a relevant context for assessing the consequences of CCDC167 loss in a disease-relevant setting.
CCDC167 is recognized as a putative tumor suppressor involved in cell cycle control and proliferation. It functions downstream of the TP53 tumor suppressor, a master regulator of genomic stability and stress responses. Upon activation, TP53 transcriptionally upregulates CCDC167, which then modulates the expression of key downstream targets, including the cyclin-dependent kinase inhibitor CDKN1A (p21) and the pro-apoptotic factor BAX. Through these interactions, CCDC167 participates in p53-mediated cell cycle arrest and apoptosis. The signaling network also involves representative pathway components such as cyclin D1 (CCND1), cyclin-dependent kinase 4 (CDK4), and retinoblastoma protein (RB1), all critical for G1/S cell cycle transition. Thus, CCDC167 deletion disrupts this regulatory axis, potentially leading to unchecked cell proliferation.
In the A2780 cellular context, knockout of CCDC167 is expected to abrogate its tumor suppressive functions, resulting in enhanced proliferative capacity and reduced apoptotic response. This perturbation likely compromises p53-mediated cell cycle arrest, thereby promoting ovarian cancer progression. Given the cisplatin-sensitive nature of the parental A2780 cells, the CCDC167 knockout model may exhibit altered drug sensitivity, offering a platform to dissect the interplay between CCDC167 and DNA damage response pathways. Consequently, this model serves as a relevant tool for mechanistic studies in ovarian cancer biology and therapeutic resistance.
The CCDC167 Knockout A2780 Polyclonal Cells are applicable to a variety of experimental paradigms, including the investigation of CCDC167??s role in ovarian cancer, apoptosis, and proliferation studies. Typical assays such as Western blotting and RT-qPCR can verify target gene disruption and changes in expression of downstream effectors like TP53, CDKN1A, and BAX. Functional readouts include cell proliferation assays (e.g., MTT), apoptosis detection via Annexin V staining, and cisplatin sensitivity testing. Additionally, migration and invasion assays can assess metastatic potential. This polyclonal knockout model is an invaluable resource for drug screening and elucidating CCDC167-related signaling mechanisms. For ordering or technical inquiries, please contact Ascent Research.
