The ARHGAP35 Knockout A-549 Polyclonal Cells product comprises a population of human A-549 lung adenocarcinoma cells that have been subjected to CRISPR/Cas9-mediated disruption of the ARHGAP35 gene, generating a heterogeneous pool of edited alleles. This polyclonal knockout cell population serves as a versatile loss-of-function model for investigating the biological roles of the p190A RhoGAP protein in non-small cell lung cancer biology. The use of a polyclonal format preserves genetic diversity and mitigates clonal artifacts, making it suitable for pooled functional screens, pathway analysis, and comparative studies against parental or control cell populations.
The A-549 host cell line, derived from a human lung adenocarcinoma, provides a well-characterized epithelial model for non-small cell lung cancer (NSCLC). These cells harbor activating mutations in KRAS and exhibit typical features of malignant lung epithelial cells, including robust proliferation, anchorage-independent growth, and invasive capacity. As a widely used NSCLC model, A-549 cells are instrumental in studying oncogenic signaling, drug response, and mechanisms driving tumor progression and metastasis, offering a clinically relevant background for ARHGAP35 functional analysis.
ARHGAP35 encodes p190A RhoGAP, a GTPase-activating protein that stimulates GTP hydrolysis of RhoA, Rac1, and Cdc42, converting them to inactive GDP-bound states. Its activity is regulated by Src family kinases, EGFR, PDGFR, and integrins, and mediated through complexes with p120 RasGAP, cortactin, filamin A, paxillin, and FAK. This regulation modulates actin cytoskeleton organization, focal adhesion turnover, and cell migration by balancing RhoA/ROCK contractility and Rac1/Cdc42 protrusions. Loss of ARHGAP35 disrupts these processes, promoting unchecked signaling and enhanced invasive potential.
In the A-549 lung adenocarcinoma context, ARHGAP35 is considered a putative tumor suppressor, with loss-of-function likely contributing to tumor progression. This polyclonal knockout population enables researchers to directly assess the impact of ARHGAP35 deficiency on NSCLC-relevant phenotypes, such as anchorage-independent growth, migration, and invasion. It provides an ideal system to dissect how ARHGAP35 intersects with core oncogenic pathways in lung adenocarcinoma, including EGFR and integrin signaling, and to evaluate its role in modulating sensitivity to targeted therapies or chemotherapeutics.
This knockout product supports a wide range of applications including Rho GTPase activation assays, scratch wound and Transwell migration/invasion assays, immunofluorescence imaging of actin and adhesion structures, and transcriptomic or proteomic profiling. It is valuable in drug sensitivity screens, tumor suppressor validation, and metastasis research in lung adenocarcinoma. For further details or to request custom services, please contact Ascent Research.
