Candida albicans, a common fungal species in the human oral cavity, has been increasingly implicated in the pathogenesis of oral tumors. Its ability to form polymicrobial biofilms is of particular concern, as these biofilms release effluents that can influence the behavior of oral epithelial cells. Emerging evidence suggests that these biofilm effluents contribute to the malignant transformation of oral keratinocytes, the primary epithelial cells lining the oral mucosa. Specifically, studies have shown that these secretions can disrupt the adhesion of oral squamous carcinoma cells to the extracellular matrix and stimulate pro-inflammatory cytokine production, including interleukins IL-6 and IL-8. Such cytokine activity is known to foster a microenvironment conducive to tumor progression and immune evasion.

This study synthesizes current findings on the mechanistic role of Candida albicans in oral carcinogenesis, with a focus on biofilm interactions and immune modulation. By examining how fungal biofilms alter cellular adhesion properties and inflammatory signaling, we highlight a critical pathway through which C. albicans may enhance tumor development in the oral cavity. The results underscore the importance of monitoring fungal infections in patients at risk of oral cancers and suggest that antifungal strategies may have potential as adjunct therapies in oral cancer management