CCSER1 Knockout A2780 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population specifically engineered for loss-of-function studies of the CCSER1 tumor suppressor gene. This product is generated by CRISPR/Cas9-mediated gene disruption in the A2780 human ovarian carcinoma cell line, yielding a heterogeneous population that captures a broad spectrum of editing outcomes without the bias of single-cell cloning. The polyclonal format offers a robust system for dissecting CCSER1 functions in epithelial ovarian cancer and for evaluating downstream molecular consequences in a disease-relevant setting.
The A2780 cell line is an established human ovarian endometrioid adenocarcinoma model derived from an untreated patient. It faithfully recapitulates key features of ovarian carcinoma, including responsiveness to clinically relevant chemotherapeutics such as cisplatin and paclitaxel. This well-characterized background is widely employed in tumor biology research, drug response profiling, and signal transduction studies, providing a reliable context for interpreting phenotypic changes resulting from CCSER1 knockout.
CCSER1 operates as a putative tumor suppressor with critical roles in cell cycle regulation, apoptosis, and cell migration. Its function is mechanistically linked to TP53-dependent pathways, responding to DNA damage signals transduced by upstream kinases ATM and ATR. CCSER1 promotes transcription of the cyclin-dependent kinase inhibitor CDKN1A (p21) and influences the balance of BCL2 family members such as BAX, thereby regulating CASP3-mediated apoptosis. Loss of CCSER1 may therefore impair these controls, leading to enhanced survival and proliferation. Additionally, CCSER1 intersects with the PI3K/AKT pathway via AKT1 and interacts with microtubule-associated proteins and actin cytoskeleton regulators, suggesting involvement in cytoskeletal organization and cell motility.
Knockout of CCSER1 in A2780 cells establishes a powerful model for investigating tumor suppressor mechanisms in ovarian carcinoma. The anticipated increase in proliferative capacity, resistance to apoptosis, and altered migration/invasion phenotypes reflect the loss of a negative growth regulator. These phenotypic alterations facilitate the dissection of ovarian cancer progression and enable the identification of therapeutic vulnerabilities, including altered sensitivity to standard-of-care agents like cisplatin and paclitaxel and potential synthetic lethal interactions.
Researchers can utilize CCSER1 Knockout A2780 Polyclonal Cells in a wide array of functional assays. Proliferation (MTS) and apoptosis (Annexin V) assays quantify growth and cell death, while Transwell assays evaluate migration and invasion. Flow cytometry permits detailed cell cycle profiling, and drug sensitivity screening with chemotherapeutics or targeted compounds is a key application. These cells are also amenable to global transcriptomic analyses by RNA-seq and biochemical confirmation via western blotting and RT-qPCR. For additional information, please contact Ascent Research.
