Microbiota and cancer: Elucidating the role of Candida albicans in cancer progression

Table 1 summarizes the mechanisms through which Candida albicans contributes to carcinogenesis[30-63]

Fungus	Associated cancer	Main hypothetical molecular mechanisms
C. albicans	Oral cancer	The main hypothesized molecular mechanisms of OC include C. albicans promoting cancer progression by producing carcinogenic byproducts, triggering inflammatory responses, inducing T-helper 17 responses, and facilitating epithelial-mesenchymal transition. Specifically, activation of the IL-17A/IL-17 receptor A-macrophage axis attracts M2-type macrophages, inducing an immunosuppressive microenvironment and promoting tumor development. Additionally, C. albicans may reduce the effectiveness of immunotherapy and influence the tumor immune microenvironment
	Esophageal cancer	C. albicans induces chronic inflammation, disrupts the esophageal mucosal barrier, promotes dysbiosis and microbial imbalance, and directly or indirectly accelerates the progression of esophageal cancer
	Gastric cancer	C. albicans reduces fungal diversity and abundance in the stomach, leading to gastric microbiome imbalance and promoting the development of GC. Additionally, its cell-free supernatant exhibits anti-tumor activity against gastric cancer cells by inducing apoptosis, inhibiting the survivin gene, and downregulating IL-8 and nuclear factor kappa-B expression, affecting inflammation and tumor growth, with potential therapeutic value
	Colorectal cancer	C. albicans activates the epidermal growth factor receptor/toll-like receptor 2-extracellular signal-related kinase/nuclear factor kappa-B-hypoxia inducible factor-1α signaling pathway, inducing a hypoxic response and promoting CRC progression. Meanwhile, studies suggest that its metabolite mixture may have a protective effect on CRC by influencing cellular energy metabolism. Additionally, C. albicans probiotics might exhibit anti-tumor effects against CRC, though the exact mechanisms remain unclear
	Breast cancer	C. albicans may influence BC by promoting tumor progression and metastasis. However, metastatic breast cancer cells have been observed to phagocytose C. albicans
	Cervical cancer	C. albicans and other microbial infections cause DNA damage and mutations, promoting CC development and increasing drug resistance

OC: Oral cancer; C. Albicans: Candida albicans; IL: Interleukin; GC: Gastric cancer; CRC: Colorectal cancer; BC: Breast cancer; CC: Cervical cancer.