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TRIM8 plays a key role in controlling the p53 molecular switch that sustains the transcriptional activation of cell cycle arrest genes and response to chemotherapeutic drugs. TRIM8 protein is able to interact with wild type p53 displacing its binding to MDM2 and consequently inducing specific post-translational modifications that stabilize and activate p53 protein. TRIM8 deficit dramatically impairs p53-mediated cellular responses to chemotherapeutic drugs and its re-expression is able to sensitize cells to treatments following p53 pathway re-activation, both in a cellular model of clear cell Renal Cell Carcinoma (ccRCC) and colorectal carcinoma (CRC). Therefore TRIM8 may represent a new promising therapeutic target in the treatment of ccRCC and CRC as well as other tumors that express a wild type p53 protein (but that show the inactivation in the functional p53 network). The study of TRIM8 structure also gives important informations on how it finely supports p53 activity, counteracting tumor progression.
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