The HAX1 Knockout CAL-27 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal population derived from the CAL-27 oral squamous cell carcinoma line, featuring targeted disruption of the HAX1 gene. This product provides a heterogeneous knockout cell pool without single-cell cloning, reducing clonal artifacts and mimicking genetic variation seen in tumor populations. The cells are suitable for bulk functional assays where knockout diversity enhances phenotypic robustness.
The parental CAL-27 cell line, established from a human tongue squamous cell carcinoma, is a well-characterized epithelial tumor model widely used to study oral cancer invasion, metastasis, and drug responses. CAL-27 retains malignant keratinocyte features, including anchorage-independent growth, providing a clinically relevant background for isogenic knockout studies. HAX1 disruption in this context enables dissection of molecular mechanisms driving oral squamous cell carcinoma progression.
HAX1 is a mitochondrial and cytoplasmic anti-apoptotic protein that interacts with SLC25A6 (ANT3) to stabilize mitochondrial membrane potential, preventing cytochrome c release and caspase activation. It also binds cortactin to regulate actin dynamics and cell migration. Upstream, HAX1 is activated by Src family kinases and IL-2 signaling, downstream of cytokine and integrin receptors. It forms complexes with HCLS1 and PKD2 and cooperates with BCL-2 family proteins. Thus, HAX1 integrates survival signals with cytoskeletal reorganization, promoting apoptosis resistance and motility.
In oral squamous cell carcinoma, elevated HAX1 expression correlates with apoptosis resistance and enhanced metastatic potential. Disruption of HAX1 in CAL-27 polyclonal cells creates a loss-of-function model to dissect the gene’s role in sustaining mitochondrial integrity and cortactin-driven migration under genotoxic or growth factor stress. Importantly, HAX1 mutations underlie Kostmann syndrome (severe congenital neutropenia), making this knockout relevant for probing shared survival mechanisms between cancer and leukopenia. This polyclonal system is ideal for identifying vulnerabilities exploitable in both hyperproliferative and cytopenic conditions.
Typical applications include western blotting for HAX1 and cleaved caspases, annexin V apoptosis assays, and cell viability testing under drug treatment. Transwell migration and invasion assays assess metastatic potential, while co-immunoprecipitation studies examine HAX1 interactions with cortactin and SLC25A6. Mitochondrial morphology can be visualized by immunofluorescence, and RNA-seq provides global transcriptomic profiles. The cells are suitable for high-throughput screening of inhibitors targeting HAX1-dependent survival pathways. For further information and technical support, please contact Ascent Research.
