The Tmem176b Knockout CT26 Cell Line is a CRISPR/Cas9-edited murine colon carcinoma cell line with disrupted Tmem176b gene. It provides a stable knockout model for studying TMEM176B function in colorectal cancer immunology and inflammasome biology. This engineered cell line abolishes TMEM176B expression, offering a robust platform to investigate cellular and molecular consequences of gene deficiency in a well-characterized tumor background.
The CT26 host cell line originates from a BALB/c mouse colon carcinoma and is a standard syngeneic model for colorectal cancer. Its adherent epithelial nature, rapid proliferation, and tumorigenic capacity in immunocompetent BALB/c mice make it ideal for preclinical cancer immunotherapy research. The BALB/c background allows assessment of immune responses and tumor-immune interactions, enabling therapeutic evaluation.
TMEM176B is an ion channel protein that negatively regulates dendritic cell (DC) maturation and NLRP3 inflammasome activation by modulating ion homeostasis. It acts downstream of TLR ligands, TNF-??, and IL-1??, and is influenced by NF-??B signaling. TMEM176B interacts with NLRP3 and ASC to restrain caspase-1 activation and IL-1?? secretion. In the TLR4/MyD88/NF-??B pathway, it functions as an inhibitory checkpoint dampening DC-driven T-cell responses. Knockout of Tmem176b enhances DC maturation, elevates inflammasome activity, and boosts IL-1?? production.
In colorectal cancer, TMEM176B may shape the tumor immune microenvironment by controlling innate immunity. CT26 tumors are inflamed and immunotherapy-responsive; thus, Tmem176b deletion likely alters dendritic cell function and inflammasome-dependent cytokine release, potentially enhancing anti-tumor immunity. This model helps dissect TMEM176B’s role in tumor growth, immune infiltration, and checkpoint inhibitor response, with relevance to inflammatory and autoimmune diseases.
Research applications include tumor immunology, inflammasome biology, and cancer immunotherapy studies. Typical assays are western blotting and RT-qPCR for knockout validation, ELISA for IL-1??, flow cytometry for DC maturation markers (CD80, CD86), co-immunoprecipitation for NLRP3/ASC interactions, caspase-1 activity assays, and in vivo syngeneic tumor growth experiments. Migration/invasion assays further assess metastatic potential. For technical inquiries, contact Ascent Research.
