The MYG1 Knockout HCT 116 Polyclonal Cells are a CRISPR/Cas9-edited human polyclonal knockout cell population designed to disrupt the MYG1 gene. This loss-of-function model enables the study of MYG1-dependent mitochondrial RNA processing without introducing a clonal bias, preserving the natural genetic heterogeneity of the host cell line. The polyclonal format is particularly suited for functional genomics screens and assays where population-level effects are preferred over isolated monoclonal phenotypes.
HCT 116 is a widely utilized human colorectal carcinoma epithelial cell line derived from a male patient. It is characterized by a near-diploid karyotype, high microsatellite instability (MSI) due to MLH1 deficiency, and activating mutations in KRAS, PIK3CA, and CTNNB1. These features make HCT 116 a well-established model for colorectal cancer research, especially for exploring oncogenic signaling pathways, mismatch repair defects, and tumor metabolism.
MYG1 encodes a mitochondrial 3′-5′ exoribonuclease that is essential for RNA surveillance and mitochondrial ribosome biogenesis. The enzyme functionally interacts with the SUPV3L1 helicase and PNPT1 polynucleotide phosphorylase within a degradosome complex, and its expression is transcriptionally regulated by PPARGC1A (PGC-1??) and NRF1. By ensuring the proper processing and stability of mitochondrial-encoded mRNAs, including MT-ND1 and MT-CO1, MYG1 directly supports the fidelity of mitochondrial translation and respiratory chain assembly.
In the HCT 116 background, MYG1 knockout compromises mitochondrial RNA quality control, leading to the accumulation of aberrant mitochondrial RNA species and defective respiratory chain function. This disruption can significantly alter cellular bioenergetics and may enhance metabolic vulnerabilities associated with KRAS-driven growth. The polyclonal knockout population thus provides a physiologically relevant system to examine how mitochondrial dysfunction intersects with oncogenic signaling in colorectal cancer cells.
This product is a powerful tool for investigating mitochondrial RNA biology, cancer metabolism, and the role of mitochondrial dysfunction in disease progression. Typical applications include mitochondrial RNA stability analysis via RT-qPCR, mitochondrial translation assays, Seahorse respirometry to assess oxidative phosphorylation, Western blotting of respiratory chain subunits, flow cytometry for mitochondrial mass, and apoptosis assays. For further technical information, please contact Ascent Research.
