The ABL1 Knockout HCT 116 Polyclonal Cells consist of a CRISPR/Cas9-edited polyclonal knockout cell population of human HCT 116 colorectal carcinoma cells with targeted disruption of the ABL1 gene. This heterogeneous pool captures diverse ABL1 knockout alleles, minimizing clonal bias and enabling robust functional studies. It serves as a versatile loss-of-function model for investigating ABL1-mediated signaling, therapeutic resistance, and tumor biology.
The HCT 116 cell line is a colorectal carcinoma epithelial line harboring oncogenic KRAS (G13D) and CTNNB1 (stabilized ??-catenin) mutations, CDKN2A (p16INK4a) deletion, and wild-type TP53, resulting in constitutive MAPK and WNT pathway activation. This genetic profile and its adherent growth, high transfectability, and reproducible drug sensitivity make HCT 116 a standard model for cancer biology and preclinical drug testing.
ABL1 is a non-receptor tyrosine kinase that integrates signals from integrins, EGFR, PDGFR, and SRC family kinases, and is activated by ATM kinase upon genotoxic stress. It directly phosphorylates substrates including CRK, CBL, STAT5, JUN, TP53, and CTNNB1 to control proliferation, survival, and migration. ABL1 interacts with GRB2, NEDD9, 14-3-3, and BRCA1, and orchestrates cytoskeletal remodeling via RAC, RHOA, and FAK, ultimately regulating MAPK1/3 (ERK1/2), AKT, and JNK cascades.
Knockout of ABL1 in HCT 116 disrupts integrin and growth factor signaling, reducing cell proliferation and migration and increasing susceptibility to apoptosis. Given the cell line??s reliance on KRAS-MAPK and ??-catenin-driven transcription, ABL1 loss impairs adaptive responses to oxidative and genotoxic stress, potentially creating synthetic lethal interactions. The wild-type TP53 status further enables studies of DNA damage repair and sensitivity to ABL kinase inhibitors such as imatinib and dasatinib.
Researchers can utilize these cells in Western blotting for phospho-ABL1 (Y412) and downstream effectors, MTT or CellTiter-Glo proliferation assays, transwell migration and invasion assays, phospho-kinase arrays, and immunofluorescence. Apoptosis detection by Annexin V staining, co-immunoprecipitation of protein complexes, and drug sensitivity screening with targeted agents allow comprehensive mechanistic dissection. These applications support research on cancer signaling, drug resistance, DNA damage response, and integrin biology. For further technical information, please contact Ascent Research.
