The ITGB1 Knockout CAL-27 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal population derived from the CAL-27 human tongue squamous cell carcinoma line, featuring targeted disruption of the ITGB1 gene. This loss-of-function model ablates integrin beta-1 expression at the population level, enabling functional interrogation of ITGB1-dependent processes. The polyclonal format preserves cellular heterogeneity and avoids clonal selection biases, better reflecting native tumor variability. Cells are supplied as a validated pool suitable for direct use in downstream molecular and cellular assays.
CAL-27 is an adherent epithelial cell line established from a tongue squamous cell carcinoma of a 56-year-old male patient. It is a widely used model in head and neck cancer research, displaying aggressive characteristics including anchorage-independent growth, invasive capacity, and oncogenic signaling pathway activation. The cell line endogenously expresses ITGB1 and its alpha integrin partners, providing a clinically relevant platform to study integrin-mediated adhesion and signaling. Its tumorigenic properties and responsiveness to extracellular matrix cues make it particularly suitable for dissecting mechanisms of local invasion and metastasis.
Integrin beta-1 (ITGB1) encodes a transmembrane receptor that heterodimerizes with alpha integrin subunits (ITGA1?CITGA11, ITGAV) to bind fibronectin, laminin, and collagen. Ligand engagement recruits talin and kindlin, promoting integrin clustering and formation of focal adhesions containing vinculin, paxillin, and ILK. This activates FAK and Src, which trigger downstream Ras?CRaf1?CMEK1/2?CMAPK1/3 (ERK1/2) and PI3K?CAKT1 pathways, and small GTPases Rac1, RhoA, Cdc42. Upstream regulators EGF, TGF-beta, HIF-1??, SP1, AP-1, and NF-??B control ITGB1 transcription, while matrix stiffness modulates activation. ITGB1 signaling upregulates Cyclin D1 and MMP2/MMP9, promoting proliferation, migration, and invasion.
In oral squamous cell carcinoma, ITGB1 overexpression is associated with tumor aggressiveness, metastasis, and therapy resistance. The ITGB1 Knockout CAL-27 Polyclonal Cells thus provide a relevant model to dissect how loss of integrin beta-1 alters focal adhesion dynamics and downstream oncogenic signaling. This knockout enables side-by-side comparison of ITGB1-proficient and ITGB1-deficient states, facilitating the identification of compensatory adhesion mechanisms and alternative survival pathways. Researchers can employ this model to investigate matrix-dependent signaling, anchorage-independent growth, and invasive behavior in a tongue cancer context.
Typical applications include adhesion and migration assays, immunoblotting for phospho-FAK (Tyr397), phospho-AKT (Ser473), and phospho-ERK1/2 (Thr202/Tyr204), and flow cytometric assessment of integrin surface expression. The cells are compatible with RT-qPCR, Western blotting, co-immunoprecipitation, apoptosis and proliferation assays, and drug sensitivity profiling. This knockout pool is also suited for tumor xenograft studies and integrin-targeted drug screening. For additional information or quality control data, please contact Ascent Research.
