The ACTA2 Knockout A2780 Polyclonal Cells are a CRISPR/Cas9-edited population of A2780 human ovarian carcinoma cells harboring a disrupted ACTA2 gene, encoding ??-smooth muscle actin. As a polyclonal knockout pool, this reagent provides a heterogeneous loss-of-function model, enabling studies where clonal variability is not a requirement and where bulk population responses are informative. The product is designed for investigating the roles of ??-SMA in cytoskeletal organization and cell behavior.
A2780 is an epithelial ovarian carcinoma cell line established from an untreated patient, widely employed in cancer research for its well-characterized tumorigenic properties, including the ability to form tumors in vivo. Its epithelial and adherent nature, combined with responsiveness to cytokines such as TGF-??1, makes it particularly suitable for studying processes like epithelial-mesenchymal transition, metastasis, and tumor?Cstroma interactions.
The ACTA2 gene encodes ??-smooth muscle actin (??-SMA), a core component of actomyosin contractile machinery in smooth muscle and myofibroblasts. Its expression is activated by TGF-??1 via SMAD2/3, with additional inputs from YAP/TAZ, mechanical stress, and angiotensin II. ??-SMA filaments interact with myosin II, tropomyosin, caldesmon, ??-actinin, and vinculin to drive contraction, matrix remodeling, and motility. Disruption of ACTA2 compromises actin cytoskeleton integrity, attenuating myofibroblast differentiation and TGF-??-mediated fibrotic/invasive responses.
In A2780 ovarian carcinoma cells, ACTA2 knockout provides a tool to dissect the role of ??-SMA in TGF-??-driven epithelial-mesenchymal transition and cancer cell migration. The A2780 line??s responsiveness to TGF-??1 allows assessment of how loss of ACTA2 alters cytoskeletal reorganization and signaling downstream of TGF-?? receptors, potentially impacting metastatic behavior and mechanotransduction via YAP/TAZ.
Typical applications include fibrosis studies using collagen gel contraction and TGF-?? stimulation assays to evaluate myofibroblast functional capacity, cancer biology experiments employing scratch wound and transwell migration assays to quantify cell motility, and cytoskeleton visualization by immunofluorescence. Validation methods like western blotting and qPCR confirm ACTA2 depletion, while co-immunoprecipitation approaches can assess interactions with myosin II or tropomyosin. This knockout pool also supports research into actomyosin-driven processes in wound healing and vascular biology. For technical inquiries, please contact Ascent Research.
