The ATAD3A Knockout NCI-H1703 Polyclonal Cells product provides a CRISPR/Cas9-edited polyclonal knockout cell population derived from the NCI-H1703 human lung adenocarcinoma epithelial cell line. This loss-of-function model disrupts the ATAD3A gene, enabling investigation of its roles in mitochondrial biology and cancer. The polyclonal format preserves a heterogeneous knockout population that avoids clonal selection artifacts and is well-suited for functional studies requiring a representative genetic background.
NCI-H1703 is a widely used non-small cell lung cancer cell line established from a lung adenocarcinoma. It retains epithelial characteristics and is a relevant model for studying mitochondrial adaptations in tumor cells. The lung adenocarcinoma origin makes this line particularly useful for exploring how mitochondrial protein alterations contribute to cancer progression, metabolic reprogramming, and therapeutic vulnerabilities.
ATAD3A is an inner mitochondrial membrane protein essential for maintaining cristae structure and intracellular cholesterol distribution. It is regulated by transcription factors NRF1 and PGC-1?? and physically interacts with MICOS complex components MIC60 (IMMT), CHCHD3, and SAMM50. ATAD3A functionally links to apoptotic regulators BAX and BCL2, and its disruption impairs mitochondrial respiratory chain complex activity. Downstream, loss of ATAD3A leads to altered mitochondrial dynamics involving DRP1, MFN1, OPA1, and activation of caspase-3 (CASP3), ultimately sensitizing cells to apoptosis.
In the context of NCI-H1703 cells, ATAD3A knockout may exacerbate mitochondrial dysfunction, disrupt cholesterol trafficking, and lower the threshold for apoptotic induction. This model is valuable for dissecting the contribution of mitochondrial ultrastructure to lung adenocarcinoma cell fitness and for testing compounds that target mitochondrial vulnerabilities. It provides a platform to study how ATAD3A-dependent cristae organization affects tumor cell survival and response to therapy.
Researchers can apply this polyclonal knockout cell population to a range of experimental paradigms, including cancer biology, mitochondrial dysfunction studies, drug sensitivity screening, and apoptosis mechanism research. Representative assays include Western blotting for ATAD3A, RT-qPCR of downstream genes, JC-1 mitochondrial membrane potential measurement, Annexin V apoptosis staining, immunoprecipitation of MICOS complexes, and Seahorse metabolic flux analysis. For further details or to discuss custom gene-editing projects, please contact Ascent Research.
