The INHBE Knockout A2780 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population targeting the human INHBE gene in the A2780 ovarian carcinoma cell line. This product consists of a heterogeneous pool of cells carrying diverse INHBE loss-of-function mutations introduced by CRISPR/Cas9-mediated gene disruption. The polyclonal format preserves genetic variability, enabling robust functional studies of gene disruption across a population rather than a single clone.
The parental A2780 is an adherent human ovarian carcinoma cell line derived from an untreated patient with ovarian endometrioid adenocarcinoma. It is a well-established model for ovarian cancer research, owing to its defined growth characteristics and retained expression of TGF-?? superfamily signaling components. This makes it an ideal host for investigating the role of inhibin E in cancer biology.
INHBE encodes inhibin beta E, which forms inhibin E by heterodimerizing with INHA. Inhibin E antagonizes activin signaling by competing for receptor binding with the help of betaglycan (TGFBR3), thereby suppressing ACVR2A/ACVR1B-mediated phosphorylation of SMAD2/3. Upstream regulators like HNF4A and activin A govern INHBE expression, while downstream targets include phospho-SMAD2/3, FST, and IGBP. In this knockout, loss of inhibin beta E abolishes inhibin E production, releasing the inhibitory constraint on activin-driven SMAD2/3 activation and altering downstream gene expression programs that control cell proliferation and metabolism.
In A2780 ovarian carcinoma cells, INHBE knockout allows researchers to dissect the functional importance of inhibin E in regulating cancer cell behavior. Enhanced activin signaling may reveal context-dependent effects on proliferation, epithelial-mesenchymal transition, or metabolic adaptation. The model also enables studies of compensatory mechanisms involving other TGF-?? family modulators like follistatin (FST). Thus, these cells provide a physiologically relevant platform for evaluating inhibin E as a potential tumor suppressor or metabolic modulator in ovarian cancer.
These INHBE knockout polyclonal cells support a broad range of assays, including western blotting for phospho-SMAD2/3, RT-qPCR for activin-responsive genes, and cell proliferation assays. SMAD-dependent luciferase reporters and co-immunoprecipitation confirm pathway activation and loss of INHBE-INHA interaction, respectively. They are also suitable for metabolic analyses and drug screens targeting TGF-?? receptor signaling. For further information or custom assay development, please contact Ascent Research.
