The ACTA2 Knockout 769-P Polyclonal Cells product consists of a CRISPR/Cas9-edited polyclonal knockout cell population derived from the 769-P human renal cell carcinoma cell line, featuring targeted disruption of the ACTA2 gene. This loss-of-function model provides a genetically heterogeneous pool of cells with ACTA2 gene ablation, enabling robust analysis of alpha-smooth muscle actin function in cancer and fibrosis contexts.
The 769-P cell line originates from a primary clear cell adenocarcinoma of the kidney and is widely employed as an epithelial cancer model in renal cell carcinoma research. These cells maintain characteristic features of the tumor microenvironment, making them particularly relevant for studying cancer-associated fibroblast activation and extracellular matrix remodeling. The 769-P line has been extensively characterized for its signaling pathways and response to TGF-?? stimulation.
ACTA2 encodes alpha-smooth muscle actin (??-SMA), a hallmark protein of myofibroblasts and smooth muscle cells that is integral to cytoskeletal organization and contractile function. Its expression is tightly regulated by TGF-??1 signaling through the TGFBR1/SMAD2/3/4 cascade and by Rho GTPase-dependent activation of serum response factor (SRF) and its co-activators myocardin and MRTF-A/B. Alpha-SMA interacts with ??-actin, myosin, tropomyosin, caldesmon, and filamin A to form contractile actomyosin bundles, linking the cytoskeleton to focal adhesion complexes and extracellular matrix components. This network mediates cell migration, force generation, and structural integrity, placing ACTA2 at the intersection of mechanical and biochemical signaling pathways.
In the 769-P renal cancer background, knockout of ACTA2 disrupts the actin cytoskeleton and impairs contractile and migratory capabilities, providing a valuable system to dissect the role of ??-SMA in epithelial-to-mesenchymal transition, tumor cell invasion, and the regulation of the tumor microenvironment. Since renal cell carcinoma progression often involves stromal activation and fibrosis, this polyclonal knockout population allows the study of heterogeneous gene inactivation effects and mimics the variable expression observed in tumor tissues. Researchers can use these cells to explore how loss of ACTA2 affects TGF-??-mediated fibrotic responses and Rho GTPase-driven cytoskeletal dynamics.
This product is suited for a range of assays including western blotting and RT-qPCR to confirm ACTA2 disruption and downstream target changes, immunofluorescence to visualize actin filament reorganization, TGF-?? stimulation assays to evaluate pathway responsiveness, and functional phenotypic analyses such as migration and collagen gel contraction assays. Typical research applications encompass fibrosis research, cancer-associated fibroblast biology, smooth muscle differentiation studies, and drug screening for anti-fibrotic agents targeting the renal cell carcinoma microenvironment. For further information, please contact Ascent Research.
