The MYG1 Knockout 786-O Polyclonal Cells product provides a CRISPR/Cas9-edited polyclonal knockout cell population targeting the MYG1 gene in the 786-O human renal cell adenocarcinoma line. This polyclonal knockout model is generated via CRISPR/Cas9-mediated gene disruption, resulting in a heterogeneous population with MYG1 ablation, enabling robust loss-of-function studies. The knockout format is designed for researchers requiring a representative population-level phenotype in clear cell renal cell carcinoma (ccRCC) models, where MYG1??s role in mitochondrial homeostasis and tumor cell survival can be systematically interrogated.
The 786-O cell line is a widely used model of ccRCC, originally derived from a primary clear cell renal cell carcinoma of a 58-year-old male patient. 786-O cells exhibit many hallmark features of ccRCC, including constitutive HIF-2?? stabilization due to VHL inactivation, making them a physiologically relevant system for studying hypoxia-independent oncogenic signaling, metabolic reprogramming, and therapeutic responses. These cells retain epithelial morphology and are amenable to standard culture conditions, while their genetic background provides a disease-relevant context for exploring mitochondrial functions in renal oncogenesis and treatment resistance.
MYG1 encodes a mitochondrial exonuclease essential for processing mitochondrial RNA and assembling functional mitochondrial ribosomes. Within the mitochondrial matrix, MYG1 cooperates with MRPL family proteins and mitochondrial ribosomal subunits to facilitate 12S rRNA maturation and ribosome biogenesis. Its expression is regulated by master mitochondrial biogenesis transcription factors PGC-1?? and NRF1. Functional MYG1 sustains translation of mitochondrially encoded proteins, including MT-CO1 and MT-ND1 of the oxidative phosphorylation complexes. Disruption of MYG1 leads to defective mitochondrial translation, reactive oxygen species (ROS) accumulation, and activation of caspase-3-dependent intrinsic apoptosis, while also impairing cell proliferation.
In 786-O ccRCC cells, MYG1 knockout recapitulates mitochondrial deficiencies relevant to renal tumor pathogenesis. ccRCC exhibits pronounced metabolic and mitochondrial alterations tied to HIF signaling and oxidative stress. Loss of MYG1 in this background amplifies mitochondrial stress and apoptotic sensitivity, providing a platform to dissect how mitochondrial ribosome impairment intersects with oncogenic signaling and apoptosis evasion. Furthermore, since MYG1 dysregulation has been implicated in melanoma and mitochondrial disorders, this model extends its utility to cross-cancer analysis and mitochondrial disease research, allowing comparative study of mitochondrial gene expression networks across tumor types.
This polyclonal knockout cell population supports diverse research applications, including cancer biology investigations of apoptotic regulation, mitochondrial biology studies of ribosome assembly and translation, and drug target validation screens for mitochondrial tumor suppressors. Researchers can employ assays such as western blotting to confirm target protein loss, RT-qPCR for mRNA expression profiling, JC-1-based mitochondrial membrane potential measurements, ROS detection probes, caspase-3 activity assays, and MTT-based cell proliferation analyses. The loss-of-function model is particularly suited for validation experiments linking mitochondrial gene expression to cancer cell viability and cell death mechanisms. For further information, please contact Ascent Research.
