The CCPG1 Knockout A2780 Polyclonal Cells product provides a CRISPR/Cas9-edited polyclonal population with disrupted CCPG1 in the A2780 human ovarian carcinoma cell line. This loss-of-function model enables investigation of p53-mediated tumor suppression, as CCPG1 is a p53-inducible gene involved in cell cycle arrest and apoptosis. The polyclonal format ensures a heterogeneous knockout pool free from clonal artifacts, suitable for biochemical, cell-based, and pharmacological assays.
The A2780 cell line originates from an ovarian endometrioid adenocarcinoma and serves as a well-characterized epithelial model of ovarian cancer. Retaining key tumor features including wild-type TP53, it is widely employed in cancer research for evaluating drug responses, signaling mechanisms, and tumor suppressor functions. This host cell background allows direct examination of CCPG1 function within a clinically relevant oncogenic context, providing insights into how p53 target gene disruption influences ovarian carcinoma cell behavior.
CCPG1 is transcriptionally regulated by TP53 and functions downstream of this master tumor suppressor, contributing to cell cycle arrest and apoptosis in response to genotoxic stress. Within the p53 network, CCPG1 acts alongside CDKN1A (p21) and BAX to enforce growth inhibition. Upon induction by DNA damage, TP53 upregulates CCPG1, which then interfaces with cell cycle regulators and apoptotic effectors. Loss of CCPG1 attenuates these tumor-suppressive processes, enabling detailed dissection of p53 target gene contributions and feedback regulation.
In the TP53-wildtype A2780 background, CCPG1 knockout impairs p53-driven cell cycle arrest and apoptosis, thereby mimicking aspects of p53 pathway deficiency frequently observed in advanced ovarian cancers. This model isolates CCPG1-specific effects on tumor suppression without confounding TP53 mutations, enabling precise dissection of downstream signaling. It also provides a platform to investigate how loss of CCPG1 alters sensitivity to chemotherapeutic agents and targeted therapies that rely on intact p53 function.
Applications include Western blotting and RT-qPCR for CCPG1 and downstream target validation, apoptosis assays to quantify cell death induction, flow-cytometric cell cycle analysis, and drug sensitivity screening. This tool supports research into ovarian cancer biology, p53 tumor suppressor function, and mechanisms of drug resistance. For further technical details, product inquiries, or custom gene-editing services, please contact Ascent Research.
