The DIP2A Knockout A2780 Polyclonal Cells product consists of a CRISPR/Cas9-edited polyclonal population of A2780 human ovarian epithelial cancer cells carrying a targeted disruption of the DIP2A gene. This loss-of-function model is generated by introducing Cas9 nuclease and a guide RNA specific to DIP2A into the host cell line, resulting in a heterogeneous pool of knockout cells suitable for downstream applications that do not require clonal uniformity. The polyclonal format captures a range of editing outcomes, offering a robust system for studying gene function in a population context.
The A2780 cell line, derived from a patient with ovarian endometrioid adenocarcinoma, serves as a well-established epithelial ovarian cancer model. These cells exhibit sensitivity to cisplatin and are widely employed in ovarian cancer research to investigate mechanisms of tumorigenesis, chemoresistance, and metastasis. As an adherent cell line with an epithelial morphology, A2780 provides a physiologically relevant platform for dissecting signaling pathways implicated in endometrioid ovarian carcinoma.
DIP2A encodes a transmembrane protein that acts as a cell surface receptor for follistatin-like protein 1 (FSTL1), a secreted glycoprotein. Upon FSTL1 binding, DIP2A initiates intracellular signaling cascades leading to the activation of phosphoinositide 3-kinase (PI3K), protein kinase B (AKT), and mechanistic target of rapamycin (mTOR). Key downstream effectors include mTOR complex 1 targets such as ribosomal protein S6 kinase (S6K) and the regulatory associated protein of mTOR (Raptor). This axis promotes the expression of Cyclin D1 and modulates the Bcl-2/Bax ratio, thereby enhancing cell cycle progression, survival, and migration. The FSTL1?CDIP2A?CPI3K?CAKT?CmTOR signaling module is thus a critical regulator of oncogenic phenotypes.
In the A2780 background, DIP2A knockout disrupts the FSTL1-mediated activation of PI3K/AKT/mTOR signaling, potentially impairing proliferative and survival signals that drive ovarian cancer progression. Given the relevance of this pathway to endometrioid adenocarcinoma, the DIP2A knockout model provides a valuable tool for elucidating the dependency of ovarian cancer cells on FSTL1/DIP2A signaling. Loss of DIP2A function may alter cellular responses to growth factors, influence drug sensitivity, and impact invasive behavior, making this model significant for preclinical cancer research.
Researchers can employ this polyclonal knockout cell population in a variety of experimental settings, including western blotting to assess AKT phosphorylation, cell proliferation assays using MTT or CCK-8, transwell migration and invasion tests, colony formation studies, and apoptosis detection via Annexin V/PI staining. Transcriptomic analysis by RNA-seq can further reveal global gene expression changes upon DIP2A loss. Co-immunoprecipitation studies enable investigation of the DIP2A-FSTL1 interaction. This product is therefore suited for projects investigating FSTL1/DIP2A signaling in ovarian cancer, exploring PI3K/AKT pathway addiction, and screening for novel therapeutics targeting this axis. For further technical details or ordering information, please contact Ascent Research.
