Alcohol consumption modulates Candida albicans-induced oral carcinogenesis and progression.

This study aimed to determine the impact of low levels of alcohol consumption on the interaction of the oral cavity with Candida albicans , a species that is commonly found at higher levels in the oral cavities of regular alcohol consumers, patients with pre-malignant diseases, and patients with existing oral cancer (OC). The gingival squamous cell carcinoma cell line, Ca9-22, was subjected to low-level ethanol exposure before co-culture with heat-inactivated C. albicans (HICA). We performed cell viability assays, measured reactive oxygen species, and used Western blot analysis for cell death markers to examine the effect of ethanol and HICA on cells. Scratch assays and anchorage-independent growth assays were used to determine cell behavioral changes. The results showed that ethanol in combination with HICA exacerbated cell death and cell cycle disruption, delayed NF-κB signaling, increased TIMP-2 secretion, and subsequently decreased MMP-2 secretion when compared to exposure to HICA alone. Conversely, both ethanol and HICA independently increased proliferation of Ca9-22 cells in scratch assays, and in combination, increased their capacity for anchorage-independent growth. Low levels of ethanol may provide protective effects against Candida -induced inflammatory oral carcinogenesis or OC progression. • Alcohol delays and dampens the NF-κB immune response in Ca9-22 oral cancer cell line. • Alcohol increases expression of TIMP-2 and decreases MMP-2 secretion in Ca9-22 cells. • Alcohol and heat-inactivated C. albicans independently increase proliferation of Ca9-22 cells in scratch assays. • Alcohol in combination with heat-inactivated C. albicans increases anchorage-independent growth of Ca9-22 cells. [ABSTRACT FROM AUTHOR]