Oral squamous cell carcinoma is associated with many known risk factors including tobacco smoking, chronic
alcoholism, poor
oral hygiene, unhealthy dietary habits and microbial
infection. Previous studies have highlighted Candida albicans host tissue
infection as a risk factor in the initiation and progression of
oral cancer. C albicans invasion induces several cancerous hallmarks, such as activation of proto-oncogenes, induction of DNA damage and overexpression of inflammatory signalling pathways. However, the molecular mechanisms behind these responses remain unclear. A recently discovered fungal toxin
peptide,
candidalysin, has been reported as an essential molecule in epithelial damage and host recognition of C albicans
infection.
Candidalysin has a clear role in
inflammasome activation and induction of cell damage. Several inflammatory molecules such as
IL-6,
IL-17, NLRP3 and
GM-CSF have been linked to
carcinogenesis.
Candidalysin is encoded by the ECE1 gene, which has been linked to
virulence factors of C albicans such as adhesion, biofilm formation and filamentation properties. This review discusses the recent epidemiological burden of
oral cancer and highlights the significance of the ECE1 gene and the ECE1
protein breakdown product,
candidalysin in oral
malignancy. The immunological and molecular mechanisms behind oral
malignancy induced by
inflammation and the role of the toxic fungal
peptide candidalysin in oral
carcinogenesis are explored. With increasing evidence associating C albicans with oral
carcinoma, identifying the possible fungal
pathogenicity factors including the role of
candidalysin can assist in efforts to understand the link between C albicans
infection and
carcinogenesis, and pave the way for research into therapeutic potentials.