Is Candida albicans a promoting factor, rather than an inducing factor for oral cancer?

Candida albicans (C. albicans) is closely associated with cancer. Whether C. albicanscan directly induce the occurrence of oral cancer remains undetermined.

This study aimed to explore the carcinogenic potential of C. albicans in oral cancer.

Transcriptome sequencing (mRNAseq) and whole exome sequencing (WES) were performed to reveal the effects of long-term C. albicans stimulation on oral mucosa in mouse models. 4-nitroquinoline-1-oxide (4NQO), a mutagenic substance that mimics tobacco, was used to examine the combined role of tobacco smoking and C. albicans in oral carcinogenesis. Additionally, the somatic mutation landscape of chronic hyperplastic candidiasis (CHC)-a variant of oral candidiasis typically presenting with dysplasia-was characterized in biopsy tissues.

Long-term C. albicans stimulation didn't directly induce oral cancer in mouse models but significantly upregulated the expression of genes related to cell proliferation and cancer development in the oral epithelium (e.g. Mki67, Kif11, Ccna2, Ckap2, Fos, Ccnb1; P < 0.05). Analysis of somatic mutations in CHC revealed that Candida and smoking might co-contribute to this type of precancerous lesion. Furthermore, C. albicans stimulation activated signaling pathways involved in inflammation and immune response, and promoted cancer formation in mice pre-treated with 4NQO.

C. albicans alone rarely induces carcinogenesis directly but can accelerate the malignant transformation of oral mucosa when combined with smoking.