The IRGQ knockout KYSE-30 polyclonal cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the human KYSE-30 esophageal squamous cell carcinoma (ESCC) cell line. This loss-of-function model disrupts the IRGQ gene, enabling dissection of its oncogenic functions. The polyclonal format provides a heterogeneous mixture of knockouts, avoiding clonal artifacts and ensuring robustness for functional assays. The gene disruption is achieved via targeted Cas9 cleavage, creating a versatile system for cancer biology applications.
KYSE-30 was established from a well-differentiated invasive esophageal squamous cell carcinoma from a 64-year-old male. This adherent epithelial cell line exhibits rapid proliferation, migration, and invasion, serving as a physiologically relevant in vitro model for ESCC. Its consistent genetic background and stable behavior make it ideal for gene perturbation studies, reflecting key hallmarks of esophageal carcinogenesis.
IRGQ is a putative oncogene that regulates proliferation, migration, and invasion in ESCC. It is regulated upstream by miR-139-3p and activates AKT/mTOR signaling, with AKT and mTOR as direct downstream targets. CRISPR/Cas9-mediated IRGQ disruption inhibits AKT and mTOR phosphorylation, attenuating oncogenic phenotypes. Additionally, IRGQ modulates autophagy through effects on LC3 and p62, and interacts with the PI3K pathway, linking it to cell survival and homeostasis.
In the context of KYSE-30 ESCC cells, IRGQ knockout provides a disease-relevant model to elucidate IRGQ’s contribution to esophageal cancer progression. Given the high frequency of AKT/mTOR signaling aberrations and autophagy dysregulation in ESCC, this polyclonal knockout population enables direct comparison with wild-type KYSE-30 cells, revealing IRGQ-dependent malignant phenotypes. It supports validation of molecular interactions within the tumor microenvironment and evaluation of IRGQ as a potential therapeutic target for esophageal cancer.
Applications include studying IRGQ-mediated oncogenic signaling, autophagy, and drug resistance. Representative techniques are Western blotting for IRGQ, AKT, mTOR, LC3, and p62; RT-qPCR; CCK-8 proliferation assay; wound healing and Transwell migration/invasion assays; immunofluorescence; and flow cytometry for cell cycle and apoptosis. This tool supports functional genomics and preclinical drug evaluation. For customization options, contact Ascent Research.
