The ATAD3A Knockout CAL-27 Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout cell population targeting the ATAD3A gene in the human oral squamous cell carcinoma (OSCC) cell line CAL-27. This model provides a genetically disrupted ATAD3A background, enabling loss-of-function studies of mitochondrial ATAD3A function without clonal isolation, thereby maintaining population-level heterogeneity relevant for cancer research.
CAL-27 is a well-characterized adherent epithelial cell line derived from a tongue squamous cell carcinoma, commonly employed in oral cancer research to study tumor cell biology, drug response, and signal transduction. Its relevance to OSCC makes it an appropriate host for investigating mitochondrial protein function in the context of head and neck malignancies.
ATAD3A is a mitochondrial inner membrane ATPase that serves as a critical nexus for cholesterol trafficking, mitochondrial dynamics, and apoptosis regulation. Its expression is regulated by intracellular cholesterol levels and SREBP transcription factors under conditions of cellular stress. Mechanistically, ATAD3A interacts with STARD1 and CYP11A1 to facilitate cholesterol import into the mitochondrial matrix for steroidogenesis, and partners with VDAC1, DRP1, and BAX to coordinate mitochondrial fission and apoptotic thresholds. Disruption of ATAD3A in this knockout model results in altered mitochondrial cholesterol distribution, imbalanced DRP1-mediated fission, and sensitization to BAX-dependent cytochrome c release and caspase-3 activation.
In oral squamous cell carcinoma, ATAD3A is frequently overexpressed and contributes to tumor cell survival, proliferation, and chemoresistance. The polyclonal nature of this knockout population in CAL-27 cells provides a physiologically relevant system to dissect how loss of ATAD3A function disrupts mitochondrial homeostasis and influences OSCC cell behavior, including responses to conventional chemotherapeutics.
This knockout product is suited for a variety of advanced research applications, including mitochondrial cholesterol measurement, Annexin V apoptosis assays, cell proliferation analysis, MitoTracker-based mitochondrial morphology assessment, co-immunoprecipitation of ATAD3A-interacting proteins, and drug sensitivity screening. It supports mechanistic studies of mitochondrial involvement in cancer and neurodegenerative diseases such as pontocerebellar hypoplasia. For further details, contact Ascent Research.
