The DNAJC15 Knockout HGC-27 Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal population derived from the HGC-27 human gastric adenocarcinoma cell line, featuring targeted disruption of the DNAJC15 gene. This knockout model is generated using CRISPR/Cas9-mediated gene disruption, resulting in a heterogeneous pool of cells with loss-of-function mutations in the DNAJC15 locus. The polyclonal nature of this product provides a robust and cost-effective tool for functional studies without the clonal variability associated with single-cell-derived knockout lines.
HGC-27 is a widely characterized human gastric epithelial cell line originally isolated from the metastatic lymph node of a gastric adenocarcinoma patient. These cells retain key features of gastric cancer, including epithelial morphology and tumorigenic potential, making them a relevant in vitro model for studying gastric cancer biology. The HGC-27 line is particularly valuable for investigating mitochondrial function, chemoresistance, and apoptosis pathways in the context of gastric malignancy.
DNAJC15 encodes a mitochondrial J-protein co-chaperone that is essential for mitochondrial protein import and the assembly of respiratory chain complexes. It functions upstream of HspA9/mortalin and interacts with components of the TOM complex, such as TOMM20 and TOMM22, to facilitate translocation of nuclear-encoded mitochondrial proteins. DNAJC15 is also implicated in iron-sulfur cluster biogenesis, acting in concert with ISCU and frataxin. Its activity is regulated by PGC-1?? and NRF1, and is subject to promoter methylation and hypoxic conditions. Downstream, DNAJC15 is required for proper function of mitochondrial respiratory chain complex I (e.g., NDUFS1) and modulates p53-dependent apoptosis. Disruption of DNAJC15 therefore leads to impaired oxidative phosphorylation, altered aconitase activity, and increased sensitivity to apoptotic stimuli.
In gastric cancer, mitochondrial dysfunction is increasingly recognized as a contributor to metabolic reprogramming and chemoresistance. The DNAJC15 knockout in HGC-27 cells provides a physiologically relevant system to dissect the role of mitochondrial co-chaperones in cancer cell survival. Since DNAJC15 expression can be epigenetically silenced in gastric tumors, this model helps elucidate how its loss affects respiratory chain integrity, reactive oxygen species (ROS) production, and sensitivity to chemotherapeutics such as cisplatin. Consequently, it serves as a powerful platform for studying the intersection of mitochondrial biology and cancer therapy.
This polyclonal knockout cell population is suitable for a broad range of functional assays, including Western blotting to confirm protein disruption, Seahorse metabolic flux analysis to assess mitochondrial respiration, and Annexin V staining to evaluate apoptosis. It can be employed in cisplatin sensitivity testing, MTT proliferation assays, ROS measurement, aconitase activity assays, and immunofluorescence for mitochondrial morphology. Researchers investigating mitochondrial dysfunction in gastric cancer, chemosensitivity mechanisms, or apoptosis regulation will find this tool invaluable. For technical specifications and ordering information, please contact Ascent Research.
