The BCAS3 Knockout HeLa Polyclonal Cells are a CRISPR/Cas9-mediated gene disruption model that targets the BCAS3 locus in HeLa cells, yielding a heterogeneous polyclonal knockout population. This product provides a loss-of-function system for investigating the role of BCAS3 in cytoskeletal regulation, cell migration, and cancer metastasis without the need for single-cell cloning.
HeLa cells are an immortalized human epithelial line originally derived from a cervical adenocarcinoma carrying HPV18 sequences. Widely adopted in cancer research, HeLa cells exhibit robust invasive capacity and are well characterized for studies of cytoskeletal dynamics, making them a suitable host for examining pro-metastatic gene functions.
BCAS3 encodes a microtubule-associated protein that integrates signals from upstream regulators such as EGF, TGF-??, integrin activation, and Src kinase to control cytoskeletal remodeling. BCAS3 interacts with tubulin, actin, EB1, and HDAC6, and its activity promotes actin polymerization and focal adhesion turnover via downstream effectors including the Arp2/3 complex, cofilin, and FAK. These effects are mediated through Rho GTPase pathways involving Rac1, Cdc42, PAK1, and LIMK, ultimately influencing lamellipodial protrusion and adhesion dynamics.
In HeLa cells, disruption of BCAS3 expression attenuates cell migration and invasion, providing a direct cellular model of metastasis suppression. The knockout cells exhibit impaired coordination of actin and microtubule networks, leading to defective focal adhesion disassembly and reduced motility, which mirrors key aspects of anti-metastatic phenotypes.
This polyclonal knockout model is applicable to a range of experimental approaches including wound healing migration assays, Transwell invasion assays, immunofluorescence microscopy for cytoskeletal visualization, Western blotting and co-immunoprecipitation for BCAS3 interactome analysis, and proliferation assays to control for growth effects. It is well suited for drug screening initiatives aimed at identifying compounds that counteract metastatic behavior or bypass BCAS3 loss. For additional product information or technical support, please contact Ascent Research.
