The IRGQ Knockout CAL-27 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout population derived from the CAL-27 human tongue squamous cell carcinoma line. These cells carry targeted disruptions of the IRGQ gene introduced by CRISPR/Cas9, producing a heterogeneous pool of loss-of-function alleles. As a polyclonal model, they circumvent clonal artifacts and provide a stable genetic background for studying IRGQ-dependent processes. This product serves as a ready-to-use in vitro system for dissecting the roles of IRGQ in autophagy and innate immunity.
The CAL-27 line, an adherent epithelial model of oral squamous cell carcinoma (OSCC), retains tumorigenic features including deregulated proliferation, migratory ability, and apoptotic resistance. Widely used in cancer research, CAL-27 cells offer a clinically relevant platform for investigating OSCC biology. Engineering these cells to lack IRGQ enables the exploration of how autophagy-related immune mechanisms influence oral cancer progression and therapeutic response.
IRGQ is a putative GTPase of the immunity-related GTPase family that functions in autophagy-dependent innate immunity. Its expression is induced by interferon-gamma and interferon-alpha through STAT1 and IRF1 transcriptional regulation. Downstream, IRGQ participates in LC3 lipidation, p62/SQSTM1 degradation, and autophagosome formation, interacting directly with LC3/GABARAP proteins, p62, and the ATG5-ATG12 conjugation complex. IRGQ acts within a pathway that includes the ULK1 complex, Beclin1, ATG5-ATG12, and LC3-II, linking GTPase activity to autophagic membrane dynamics during immune activation.
In CAL-27 OSCC cells, IRGQ knockout disrupts autophagic flux, potentially compromising survival under metabolic stress, hypoxia, or drug treatment. Since autophagy supports tumor cell fitness and immune evasion in OSCC, this model allows investigation of IRGQ??s contribution to these processes. The polyclonal population better reflects tumor heterogeneity and avoids selection biases, making it suitable for examining variable responses to autophagy-modulating agents and interferon signaling.
Applications include studying autophagy in oral cancer, assessing immune evasion via the IRGQ?Cinterferon axis, and screening for drug sensitivities linked to autophagy. Typical assays encompass Western blotting for LC3-II and p62, RT-qPCR of IRGQ and interferon-stimulated genes, cell viability and migration/invasion tests, and co-immunoprecipitation with LC3 family members. The model is also applicable to infectious disease and autoimmune disorder research. For further information, please contact Ascent Research.
