The KANK2 Knockout HT29 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal population derived from HT29 colorectal adenocarcinoma cells with disruption of the KANK2 gene. This heterogeneous loss-of-function model consists of cells with various editing events, collectively abolishing functional KANK2 protein. The polyclonal format avoids clonal biases inherent in single-cell-derived lines, offering a robust tool to study KANK2-dependent processes in a physiologically relevant genetic background.
The HT29 cell line originates from a human colorectal adenocarcinoma and is a standard model for intestinal epithelial biology and colorectal cancer. These adherent epithelial cells retain integrin expression, polarization capacity, and differentiation potential, rendering them suitable for investigating cell adhesion, migration, drug responses, and oncogenic signaling. Their well-characterized properties make them an ideal host for gene-editing studies focused on tumor progression mechanisms.
KANK2 functions as a scaffold protein that links integrin?Ctalin complexes to the actin cytoskeleton, thereby regulating focal adhesion dynamics and cell motility. Upon integrin engagement, talin binds KANK2, which subsequently recruits actin, LPP, vinculin, and paxillin to adhesion sites. Upstream regulators such as RhoA and SRC kinases modulate this process, while downstream targets include RhoA, Rac1, FAK, and the YAP/TAZ transcriptional co-activators. KANK2 orchestrates Rho GTPase pathways, particularly RhoA/ROCK-mediated contractility, controlling adhesion maturation and cytoskeletal organization. Consequently, KANK2 knockout disrupts integrin signaling, adhesion assembly, and mechanotransduction.
In HT29 cells, KANK2 disruption enables dissection of colorectal cancer cell migration and invasion. These epithelial cells can undergo phenotypic transitions in response to micro-environmental cues; KANK2 loss alters focal adhesion scaffolding, impacting Rho GTPase activity and cytoskeletal rearrangements critical for dissemination. This model is thus valuable for probing molecular drivers of metastasis and for testing adhesion-targeted therapies.
Research applications include cancer metastasis studies, nephrotic syndrome modeling, and analysis of cell adhesion signaling. Assays such as Transwell migration/invasion, Western blotting of FAK and paxillin, immunofluorescence of vinculin and actin, and Rho GTPase activity measurements facilitate quantitative functional and mechanistic assessments. Drug sensitivity screening can additionally reveal KANK2-dependent therapeutic vulnerabilities. For additional information or application support, please contact Ascent Research.
