The Tpt1 Knockout CT26.WT Cell Line is a CRISPR/Cas9-edited knockout cell line derived from Mus musculus CT26.WT colorectal carcinoma cells. This model features targeted disruption of the Tpt1 gene, generating a stable loss-of-function system for studying translationally-controlled tumor protein (TPT1) in cancer biology. It provides a reliable platform for mechanistic and pharmacological investigations.
CT26.WT is a BALB/c mouse colorectal adenocarcinoma line chemically induced by N-nitroso-N-methylurethane. As a syngeneic tumor model, it enables in vivo studies in immunocompetent BALB/c hosts, reflecting key aspects of colorectal cancer progression, tumor microenvironment, and immune interactions. The line??s aggressive tumorigenicity makes it ideal for translational oncology research.
TPT1, encoded by Tpt1, is a multifunctional protein regulating proliferation, apoptosis, and stress responses. It is repressed by p53 and activated by mTORC1 and cellular stress. TPT1 interacts with Mcl-1, p53, Bax, and tubulin, influencing the mTOR and p53 pathways. It stabilizes Mcl-1, inhibiting apoptosis, and modulates Bcl-xL. Disruption of Tpt1 abolishes its anti-apoptotic function, enhancing p53-mediated apoptosis and impairing mTORC1 signaling, thereby sensitizing cells to stress-induced death.
In colorectal carcinoma, Tpt1 knockout disrupts apoptosis resistance, shifting signaling toward pro-apoptotic effectors like Bax and relieving Mcl-1-mediated survival. This sensitizes CT26.WT cells to chemotherapeutics such as 5-fluorouracil and oxaliplatin. Additionally, loss of the histamine-releasing factor TPT1 links the model to allergic inflammation studies, bridging tumor biology and immune regulation.
This cell line supports western blotting for Tpt1, Mcl-1, and p53; RT-qPCR; apoptosis assays (Annexin V/PI); cell viability and colony formation; xenograft tumor growth; and drug sensitivity screens. It is also suited for syngeneic immunology studies evaluating tumor-immune dynamics. For detailed product inquiries, please contact Ascent Research.
