The ITGA6 Knockout HT29 Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout cell population derived from the HT29 human colon adenocarcinoma cell line, in which the ITGA6 gene has been disrupted. This product provides a loss-of-function model for studying integrin alpha-6, a critical subunit of laminin-binding integrin heterodimers. The polyclonal nature of the knockout population captures a range of genetic edits, enabling robust assessment of ITGA6 function in a heterogeneous cellular context. Researchers can utilize these cells to investigate the role of ITGA6 in cell adhesion, migration, and signal transduction pathways relevant to epithelial biology and cancer.
HT29 is an epithelial cell line originally isolated from a 44-year-old Caucasian female with colon adenocarcinoma. It is a well-established model for colorectal cancer research, extensively employed in studies of intestinal epithelial function, drug transport, and oncogenic signaling. HT29 cells form polarized monolayers and retain features of absorptive enterocytes, making them suitable for investigating cell-matrix interactions and epithelial barrier integrity. Their widespread use in cancer biology provides a reliable platform for dissecting molecular mechanisms underlying tumor progression and therapeutic resistance.
The ITGA6 gene encodes the integrin alpha-6 subunit, which pairs with integrin beta-1 (ITGB1) or beta-4 (ITGB4) to form laminin receptors. Ligand engagement triggers intracellular signals through the FAK-Src-Akt and MAPK cascades, regulated by upstream laminins, EGF, TGF-beta, PKC, and ILK. Downstream effectors include FAK, Src, Akt, Rho GTPases, and BCL2 proteins. Key interacting partners such as CD151, laminin-332, and plectin link integrins to the cytoskeleton, ensuring hemidesmosome stability. In the absence of ITGA6, laminin-mediated adhesion and downstream survival/proliferation signals are disrupted.
In HT29 colorectal cancer cells, ITGA6 knockout abrogates laminin-dependent adhesion and integrin signaling, impacting epithelial-mesenchymal transition (EMT), anoikis resistance, and metastatic potential. Disruption of the PI3K/Akt pathway may sensitize cells to apoptosis and modulate drug responses. This model allows dissection of integrin alpha-6’s role in colon adenocarcinoma progression, facilitating studies of cell-matrix dynamics, migration, and invasion. It also provides a system to identify compensatory mechanisms activated upon loss of laminin receptor function.
These polyclonal knockout cells are suited for cancer invasion, metastasis, epithelial barrier function, and drug resistance studies. They enable validation of integrin-targeted therapies and cell-matrix interaction analyses. Representative assays include western blotting, immunofluorescence, cell adhesion and migration assays, laminin binding, flow cytometry, and anoikis assays. For further technical information or to discuss acquisition, please contact Ascent Research.
