The HAVCR1 Knockout CAL-27 Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout cell population generated from the CAL-27 human oral squamous cell carcinoma line, engineered to disrupt endogenous HAVCR1 gene expression encoding the TIM-1 protein. This gene-edited model facilitates loss-of-function studies of TIM-1 in cancer biology, immune signaling, and viral pathogenesis. The polyclonal format retains the genetic heterogeneity of the parental CAL-27 line, ensuring reproducible, population-level readouts and avoiding clonal selection biases.
CAL-27 is an epithelial carcinoma cell line originally derived from a human tongue squamous cell carcinoma prior to any treatment, and it is widely used as a model for oral squamous cell carcinoma. This cell line exhibits characteristic features of aggressive tumor cells, including dysregulated proliferation and survival pathways. Employing CAL-27 as the host for HAVCR1 knockout allows direct interrogation of TIM-1 function within a disease-relevant cellular context, where aberrant signaling networks drive malignancy. The untreated origin of CAL-27 also provides a clean genetic background, avoiding therapy-induced alterations and enabling clear interpretation of gene-specific phenotypes.
HAVCR1 (TIM-1) is a transmembrane protein that functions as a phosphatidylserine receptor mediating uptake of apoptotic cells and serves as the cellular receptor for hepatitis A virus. In T cells, TIM-1 acts as a costimulatory molecule; ligand engagement triggers association with LCK and the CD3 complex, leading to phosphorylation of ZAP70 and LAT, and subsequent activation of PI3K/AKT and MAPK/ERK pathways. Downstream, these cascades regulate transcription factors NFAT and AP-1 and promote expression of Bcl-xL. Upstream regulators include IL-4, STAT6, NF-??B, TGF-??, and HIF1??, which modulate HAVCR1 expression under inflammatory and stress conditions. TIM-1 also interacts with TIM-4 to coordinate apoptotic cell clearance, linking innate immune sensing to adaptive responses.
In CAL-27 oral cancer cells, HAVCR1 knockout disrupts TIM-1-dependent PI3K/AKT and MAPK/ERK signaling networks that control cell survival, proliferation, and potential immune evasion. Abrogation of phosphatidylserine-mediated signaling may impair nutrient acquisition from apoptotic cells in the tumor microenvironment, while loss of downstream kinase activation reduces proliferative drive and sensitizes cells to apoptosis. Consequently, this knockout model is valuable for dissecting the contributions of TIM-1 to oral squamous cell carcinoma progression and evaluating its potential as a therapeutic target. Moreover, it permits exploration of cross-talk between phosphatidylserine sensing and oncogenic pathways in epithelial cancers.
This polyclonal knockout cell product supports diverse research applications, including mechanistic studies of hepatitis A virus entry, T-cell costimulation biology, and kidney injury biomarker discovery. Oral cancer researchers can apply functional assays such as cell viability, apoptosis, and migration, coupled with phospho-AKT and phospho-ERK quantification via western blotting or flow cytometry. The cells are equally suited for RT-qPCR, immunofluorescence, and viral entry assays. These tools facilitate rigorous target validation and signaling analysis in drug development. For detailed specifications, batch data, or ordering, please contact Ascent Research.
