The ISOC2 Knockout MES-OV Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the MES-OV human ovarian cancer cell line, designed to disrupt the ISOC2 gene. This loss-of-function model enables systematic investigation of ISOC2-dependent processes in a disease-relevant background. The polyclonal format offers a heterogeneous knockout population that avoids single-cell clone artifacts, providing a robust tool for studying mitochondrial translation and its implications in ovarian cancer biology.
MES-OV is a well-characterized cell line established from an ovarian endometrioid adenocarcinoma. It faithfully recapitulates molecular and metabolic features of this histological subtype, making it a valuable model for ovarian cancer research. The line retains key signaling pathways and mitochondrial dependencies typical of endometrioid tumors, allowing researchers to assess how ISOC2 disruption influences cancer cell physiology, including metabolic reprogramming and stress responses within the native genomic and mitochondrial context.
ISOC2 encodes a mitochondrial protein essential for large mitochondrial ribosomal subunit assembly. It physically interacts with MRPL12, a core component of the 39S mitochondrial ribosome, facilitating efficient mitochondrial translation. ISOC2 expression is transcriptionally regulated by NRF1 and PGC-1??, master regulators of mitochondrial biogenesis. Downstream, ISOC2 function impacts the accumulation of MRPL12 and other mitochondrial ribosomal proteins, thereby modulating the translation of mitochondrial-encoded oxidative phosphorylation subunits. This gene operates within a network comprising MRPL12, MRPL19, MRPL45, and mitochondrial rRNA, positioning ISOC2 as a critical node in mitochondrial ribosome biogenesis.
In the MES-OV host background, ISOC2 knockout permits direct interrogation of mitochondrial translation??s role in ovarian cancer metabolism. Given the heightened dependency of cancer cells on mitochondrial function for ATP production, redox balance, and biosynthetic intermediates, disrupting ISOC2 may unmask vulnerabilities exploitable for therapeutic intervention. This model is particularly relevant for exploring mitochondrial disorders and the molecular underpinnings of Cat eye syndrome, while also serving as a platform to dissect how mitochondrial ribosome dynamics intersect with oncogenic signaling in ovarian cancer.
Typical applications include mitochondrial translation assays to measure de novo protein synthesis within mitochondria, co-immunoprecipitation with MRPL12 to confirm disrupted ribosome assembly, RT-qPCR for mitochondrial gene expression profiling, Western blotting for mitochondrial protein levels, and immunofluorescence to assess mitochondrial morphology and localization. These tools enable functional studies of mitochondrial ribosome biogenesis, mitochondrial disease modeling, and cancer metabolism research. For additional details or to request a quote, please contact Ascent Research.
