TABLE 1.

The association of C. albicans and cancers.

Fungus	Associated cancer	Main hypothetical molecular mechanisms	References
C. albicans	Oral cancers	Form biofilm, produce hydrolase, and metabolize alcohol into carcinogenic acetaldehyde.	Marttila et al., 2013; Alnuaimi et al., 2015, 2016
		Increases p63 and vimentin expression and decreases E-cadherin expression.	Lo Muzio et al., 2007; Kushwaha et al., 2019; Vadovics et al., 2022
		Zymosan from the fungal cell wall promotes the proliferation of oral squamous cell carcinoma (OSCC) cells through the TLR2/MyD88/NF-κB signaling pathway. Moreover, zymosan can promote the expression of E-cadherin, enhance the adhesion of C. albicans to OSCC cells, and further increase IL-1β production in OSCC cells, and promote cancerous inflammation.	Chen et al., 2020
		Produce endogenous nitrosamines.	Krogh, 1990
		CaADH1 gene is involved in OSCC either with or without metastasis.	Hafed et al., 2019
	Gastric cancer (GC)	Reduction in the diversity and richness of fungi in the stomach contributes to the pathogenesis of GC.	Zhong et al., 2021
	Colorectal cancer (CRC)	Enteric fungal microbiota dysbiosis and ecological alterations. Candida albicans increases glycolysis levels in macrophages through the HIF-1 pathway, prompting IL-7 secretion and release from macrophages. The increase of IL-7 effectively promotes the expression level of Stat3 and AhR transcription factors in intestinal innate lymphocytes 3 (ILC3), which then increases the level of IL-22 secretion, thus promoting the proliferation of intestinal epithelial cells and the progression of CRC.	Coker et al., 2019; Zhu et al., 2021
	Breast tumor	Induce Tregs and result in dysregulation of cytokine network and thereby facilitate tumor growth.	Ahmadi et al., 2019
	Liver cancer	Reprogramm tumor cell metabolism and contributes to the cancer progression dependent on NLRP6.	Liu et al., 2022

CaADH1, Candida albicans alcohol dehydrogenase 1; OSCC, oral squamous cell carcinoma; ILC3, intestinal innate lymphocytes 3.