The AKT3 Knockout A2780 Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout cell population derived from the A2780 human ovarian carcinoma cell line, designed for targeted disruption of the AKT3 gene. This knockout model provides a valuable tool for investigating AKT3-specific functions in oncogenic signaling, cell survival, and proliferation. The polyclonal format offers a mixed population of genetic perturbations, enabling robust assessment of AKT3-dependent phenotypes without clonal bias. Unlike a clonal cell line, this polyclonal pool maintains heterogeneity while ensuring functional loss of AKT3 at the population level.
The A2780 cell line was originally isolated from an untreated patient with ovarian endometrioid adenocarcinoma, serving as a well-established model for epithelial ovarian cancer research. These cells retain key characteristics of ovarian carcinoma, including intact PI3K-AKT pathway signaling and sensitivity to chemotherapeutic agents such as cisplatin. As an adherent epithelial cell line, A2780 provides a physiologically relevant context for studying tumor cell behavior, drug resistance, and metastatic potential. The genetic background of A2780, including wild-type TP53 status, makes it particularly suitable for dissecting AKT3-mediated survival mechanisms.
AKT3 is a serine/threonine kinase belonging to the AKT family, which is a central node in the PI3K-AKT signaling pathway. Upon activation by upstream regulators including PI3K, PDK1, and mTORC2, AKT3 translocates to the plasma membrane and phosphorylates a diverse array of downstream targets such as GSK3??, FOXO transcription factors, MDM2, and BAD, thereby promoting cell proliferation, survival, metabolism, and migration. It also inhibits apoptosis through phosphorylation of pro-apoptotic proteins and regulates cell cycle progression via p21 and p27. AKT3 activity is tightly controlled by negative regulators like PTEN and direct interactors such as APPL1, CTMP, and TRB3. The pathway components TSC1/TSC2, mTORC1, S6K, and 4E-BP1 further mediate its effects on protein synthesis and growth.
In A2780 ovarian cancer cells, aberrant AKT signaling is often associated with enhanced proliferation and chemoresistance. Knockout of AKT3 in this polyclonal population disrupts oncogenic signals downstream of PI3K, potentially reducing cell viability and sensitizing cells to apoptotic stimuli. This model enables dissection of AKT3 isoform-specific contributions versus the broader AKT family, providing insights into ovarian carcinoma pathophysiology. Given the role of AKT3 in overgrowth syndromes like MCAP, this knockout system also offers a platform to study gene-disease relationships relevant to cancer and developmental disorders.
Typical applications include studying AKT3-dependent signaling through phospho-immunoblotting of AKT, GSK3??, and S6K, and assessing functional consequences via cell proliferation (MTT/BrdU) and apoptosis (Annexin V/caspase-3) assays. The polyclonal cells are suitable for drug screening of PI3K/AKT inhibitors and for investigating mechanisms of cisplatin resistance. Migration and invasion assays (transwell) can elucidate AKT3’s role in metastasis, while RNA-seq analysis enables transcriptomic profiling. These cells serve as a critical tool for ovarian cancer research, signal transduction studies, and therapeutic development. For further information or to place an order, please contact Ascent Research.
