The IRGQ Knockout HCT 116 Polyclonal Cells product provides a CRISPR/Cas9-edited polyclonal cell population featuring targeted disruption of the IRGQ gene in the human HCT 116 colorectal carcinoma cell line. This knockout model is generated through CRISPR/Cas9-mediated gene disruption, resulting in a heterogeneous pool of cells carrying diverse loss-of-function alleles. The polyclonal format preserves population-level heterogeneity while enabling robust assessment of IRGQ-dependent phenotypes, making it suitable for applications requiring consistent knockout effects without clonal artifacts.
The host HCT 116 cell line is a widely used epithelial model of colorectal carcinoma, notable for its near-diploid karyotype and key oncogenic mutations, including KRAS G13D, TP53 deficiency, and ??-catenin stabilization. These cells exhibit high microsatellite instability (MSI-high) and display adherent morphology, closely mirroring molecular features of sporadic colorectal tumors. The well-characterized genetic background of HCT 116 provides a relevant context for investigating tumor cell biology, drug responses, and immune interactions within colorectal cancer research.
IRGQ encodes an interferon-inducible GTPase that functions at the intersection of autophagy regulation and innate immune defense. It is transcriptionally activated by type I and type II interferons (IFN-??, IFN-??, IFN-??) through the JAK-STAT signaling axis, primarily engaging IRF1, STAT1, STAT2, JAK1, and TYK2. IRGQ interacts with autophagy-related proteins, including BECN1 and members of the ATG conjugation system, and its GTPase activity influences downstream markers such as LC3-II and SQSTM1/p62, while also modulating mTORC1 signaling. It exhibits functional kinship with the IRGM family of immunity-related GTPases, mediating cellular responses to intracellular pathogens.
In the context of colorectal carcinoma, IRGQ may influence tumor cell adaptation through autophagy-dependent survival mechanisms, inflammatory signaling, and immune evasion. Its loss in HCT 116 cells??which already harbor mutations in TP53 and ??-catenin??enables dissection of IRGQ??s contribution to proliferation, apoptotic sensitivity, and autophagic flux in a cancer-relevant microenvironment. This model allows researchers to study how interferon-driven GTPase networks intersect with oncogenic pathways and could reveal vulnerabilities specific to MSI-high colorectal cancers.
This knockout model supports a broad range of experimental applications, including autophagy flux analysis using chloroquine treatment with LC3 and SQSTM1 immunoblotting, RT-qPCR profiling of interferon-stimulated genes, and drug sensitivity screening against rapamycin or chloroquine. Additional assays include IncuCyte-based proliferation monitoring, co-immunoprecipitation of IRGQ-interacting complexes, and flow cytometric evaluation of apoptosis and cell cycle alterations. Researchers can leverage this system to explore IRGQ??s role in colorectal cancer progression, innate immune signaling, and therapeutic resistance. For further technical details, please contact Ascent Research.
