The IRGQ Knockout LoVo Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the human colorectal adenocarcinoma cell line LoVo. This mixed population carries heterogeneous IRGQ gene disruptions, providing a loss-of-function model for studying the gene’s role in autophagy, innate immunity, and mitochondrial homeostasis. The polyclonal format is well-suited for bulk functional assays, pooled screens, and studies where clonal heterogeneity reflects in vivo tumor diversity.
LoVo is an epithelial cell line established from a Dukes’ type C colorectal adenocarcinoma metastasis, widely employed to investigate colorectal cancer metastasis and drug sensitivity. Its invasive phenotype and responsiveness to chemotherapeutics such as oxaliplatin and 5-fluorouracil make it an ideal host for examining how IRGQ influences autophagy-dependent survival mechanisms. This metastatic background provides a physiologically relevant context for studying migration, invasion, and tumor progression linked to innate immune signaling.
IRGQ encodes an interferon-gamma-inducible GTPase that localizes to autophagosomal membranes and mitochondria. Its expression is driven by IFNG through JAK1-STAT1-IRF1 signaling and is integrated into the autophagy pathway via interactions with ULK1, BECN1, ATG5, and MAP1LC3B. IRGQ associates with p62/SQSTM1, TECPR1, IRGM, and FIS1 to facilitate autophagosome formation and mitochondrial fission. Downstream, IRGQ modulates LC3 lipidation, p62 degradation, and the expression of BNIP3 and DNM1L, thereby regulating autophagic flux and mitochondrial quality control. Disruption of IRGQ may impair clearance of ubiquitinated cargo and mitochondria, attenuating interferon-driven innate immune responses.
In colorectal cancer, autophagy can support stress survival or promote cell death, and IRGQ’s intersection with innate immunity highlights its potential role in immune evasion. The LoVo knockout model is particularly valuable for dissecting how interferon-gamma signaling through IRGQ affects mitochondrial integrity and drug sensitivity in metastatic colon cancer. Loss of IRGQ may reveal vulnerabilities exploitable for therapeutic intervention, especially in autophagy-dependent chemoresistance.
Applications include Western blotting for LC3-I/II and p62 to monitor autophagic flux, immunofluorescence of autophagosomes, and mitophagy flow cytometry. Drug sensitivity assays with oxaliplatin and 5-FU assess chemoresistance mechanisms. Transwell migration/invasion assays and RT-qPCR for interferon-stimulated genes further elucidate IRGQ’s roles in metastasis and innate immunity. For inquiries or technical support, contact Ascent Research.
