The ARHGAP10 Knockout A-549 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population designed for loss-of-function studies of ARHGAP10. Originating from the human A-549 lung adenocarcinoma line, this product provides a heterogeneous pool of cells with gene disruption at the ARHGAP10 locus, generated via CRISPR/Cas9-mediated targeting, and is intended for immediate functional characterization without clonal isolation.
The A-549 cell line, derived from a 58-year-old male with lung adenocarcinoma, is a type II alveolar epithelial model extensively utilized in cancer biology, drug discovery, and metastasis research. Its robust growth, manipulability, and well-mapped signaling pathways make it an ideal host for investigating the role of actin-regulatory genes in tumor progression.
ARHGAP10 encodes a Rho GTPase-activating protein that specifically hydrolyzes GTP on RhoA, Cdc42, and Rac1, inactivating these molecular switches and downregulating actin cytoskeleton dynamics, focal adhesion turnover, and cell migration. ARHGAP10 activity is stimulated by upstream signals from FAK, Pyk2, integrin-mediated adhesion, and growth factor receptors, and it operates through complexes that include FAK, Pyk2, PACSIN2, dynamin-2, actin, and paxillin. Downstream, its GAP function attenuates RhoA/ROCK-mediated stress fiber formation, Cdc42/Rac1-PAK-driven protrusions, and cofilin-mediated actin severing, thereby balancing adhesive and migratory cell behaviors.
In the A-549 adenocarcinoma background, loss of ARHGAP10 function is expected to remove a critical brake on Rho GTPase activity, leading to constitutive cytoskeletal remodeling, enhanced motility, and heightened invasive capacity. This knockout model thus provides a relevant cellular context to dissect how ARHGAP10 deficiency contributes to the molecular mechanisms of lung cancer cell dissemination and to evaluate the dependence of metastatic traits on specific Rho pathway effectors.
Typical applications include Transwell migration, wound healing, and Matrigel invasion assays, coupled with Rho GTPase activity pull-downs, phalloidin-based F-actin staining, and immunoblotting for phospho-FAK and cofilin. The cell population supports anti-cancer drug target validation and functional genomic screens aimed at identifying modulators of actin dynamics and cell adhesion. For additional product details or ordering, please contact Ascent Research.
