The ABL2 Knockout HCT 116 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the HCT 116 colorectal carcinoma line. This heterogeneous ABL2-disrupted cell pool enables loss-of-function studies without clonal selection bias, maintaining genetic diversity for robust analysis of ABL2-dependent phenotypes in a cancer model.
The HCT 116 host cell line is an epithelial colorectal adenocarcinoma model from a 48-year-old male, featuring a KRAS G13D mutation, microsatellite stability, and wild-type p53. Its adherent growth and aggressive properties make it a standard for studying oncogenic signaling, tumor invasion, and metastasis. This genetic background provides a relevant setting to investigate ABL2??s role in colon cancer progression.
ABL2 is a non-receptor tyrosine kinase homologous to ABL1 that regulates actin cytoskeleton remodeling, cell adhesion, and migration. It is activated by PDGFR, integrins, Src family kinases, and reactive oxygen species, and phosphorylates downstream targets including Crk adaptors, C3G, paxillin, and cortactin. This drives Rac1-mediated actin polymerization and focal adhesion turnover, coordinated through interactions with ArgBP2 and CAP/ponsin. Key pathways include PDGFR ?? ABL2 ?? Crk/C3G ?? Rac1 ?? actin polymerization and integrin ?? FAK ?? Src ?? ABL2 ?? paxillin phosphorylation, linking extracellular cues to lamellipodia formation and invasion.
In HCT 116 cells, ABL2 knockout permits dissection of its contributions to KRAS-driven colorectal cancer phenotypes. With an activating KRAS mutation and intact p53, these cells model a prevalent tumor genotype where ABL2 may promote cytoskeletal rearrangement, adhesion dynamics, and migration. Loss of ABL2 here enables investigation of its role in oxidative stress responses and therapeutic resistance. The polyclonal knockout pool reflects tumor cell diversity, offering population-level insights into ABL2-dependent mechanisms of invasion and metastasis.
These knockout cells are suited for diverse assays, including Western blotting, Transwell migration/invasion, actin and focal adhesion immunofluorescence, co-immunoprecipitation, and kinase activity assays. They facilitate wound healing and xenograft metastasis studies, as well as drug sensitivity screens to identify ABL2-related therapeutic vulnerabilities. Additionally, the model supports target validation for colorectal and other solid tumors. Researchers can exploit this resource to link ABL2 signaling to phenotypic outcomes in cancer biology. For inquiries, contact Ascent Research.
