Cigarette smoke, saliva, the translocator protein 18 kDa (TSPO), and oral cancer.

Oral squamous cell carcinoma (OSCC) incidence is induced primarily by cigarette smoke (CS). The 5-year survival rate for advanced OSCC stands at only 20%. Studies exploring underlying mechanisms of OSCC development have suggested free radicals such as reactive oxygen species generated by CS as contributing to OSCC, with effects enhanced by transition metal ions iron and copper contained in the saliva. Located on the outer mitochondrial membrane of various cell types, the 18-kDa translocator protein (TSPO) is up-regulated under pathological conditions such as cancer and inflammation. We focused on studying the interaction between TSPO, CS, salivary effects, and OSCC. Increased TSPO expression in OSCC tumors correlates significantly with reduced patient survival rate, indicating the possible role of TSPO in OSCC pathogenesis. We speculate that TSPO in OSCC is dysfunctional or mutated, rendering it ineffective in promoting apoptosis and blocking malignant transformation. Basal, precancer lower function of TSPO may diminish the TSPO capacity for pro-apoptotic and anti-cancer activity, resulting in development of OSCC. In order to overcome this, TSPO over-expression is induced, unfortunately with no benefit, as it is a malfunctioning TSPO, similar to cases where over-expression of a mutated form of the p53 gene in tumors is associated with carcinogenesis.

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