HAX1 Knockout CAL-27 Cell Line is a CRISPR/Cas9-mediated gene-disrupted cell line derived from the CAL-27 human oral squamous cell carcinoma (OSCC) epithelial cell line. This knockout model enables functional interrogation of HAX1 (HS1-associated protein X-1), a critical anti-apoptotic factor, by eliminating its expression. Designed for biomedical research, this cell line offers a defined genetic background for dissecting HAX1-dependent mechanisms in apoptosis regulation, mitochondrial homeostasis, and cell migration. The product is provided as a purified knockout cell line generated using advanced genome-editing technology, enabling reproducible and robust loss-of-function studies.
The parental CAL-27 cell line originates from a 56-year-old male patient with tongue squamous cell carcinoma, representing a well-characterized human OSCC model. CAL-27 cells are adherent epithelial cells that retain key features of oral squamous carcinoma, including dysregulated proliferation and survival pathways, making them highly relevant for studying tumor biology. This host cell background provides a clinically pertinent context for investigating HAX1??s role in OSCC pathogenesis, particularly its contributions to apoptosis resistance and metastatic behavior, which are hallmarks of aggressive oral cancers.
HAX1 is a ubiquitously expressed anti-apoptotic protein that primarily localizes to the mitochondrial outer membrane, where it preserves mitochondrial membrane potential and prevents cytochrome c release, thereby suppressing caspase-3 activation and downstream PARP cleavage. HAX1 expression is transcriptionally upregulated by NF-??B and SP1, linking it to pro-survival signaling, while the Omi/HtrA2 protease cleaves HAX1 under apoptotic stress. Beyond mitochondrial protection, HAX1 binds cortactin and actin to regulate cytoskeletal reorganization and cell migration, with additional interactors including HCLS1, GRB7, and EB1, positioning HAX1 as a nodal integrator of apoptosis resistance and cell motility.
In OSCC, HAX1 overexpression correlates with chemoresistance and enhanced survival, highlighting its therapeutic relevance. The HAX1 Knockout CAL-27 Cell Line thus serves as a precise genetic tool to investigate HAX1’s contributions to OSCC pathophysiology, including its role in blocking mitochondrial outer membrane permeabilization downstream of Bcl-2 family proteins and its impact on PI3K/Akt-mediated survival signaling. This model further enables studies on HAX1-regulated actin reorganization, essential for OSCC invasion, and identification of synthetic lethal partners.
Key applications include Western blotting to confirm HAX1 protein loss, JC-1 staining for mitochondrial membrane potential assessment, and Annexin V/PI apoptosis assays. Transwell migration and MTT viability assays enable analysis of cell motility and drug sensitivity. Co-immunoprecipitation and immunofluorescence can be employed to study HAX1 interactions with cortactin or HCLS1. This knockout cell line is also suitable for CRISPR-based rescue experiments, high-content imaging, and screening of agents targeting the mitochondrial apoptosis pathway. For technical inquiries, please contact Ascent Research.
