The evil companion of OSCC: Candida albicans

Abstract

ObjectiveMicrobial dysbiosis and microbiome‐induced inflammation may play a role in the etiopathogenesis of oral squamous cell carcinoma (OSCC). Candida albicans (C. albicans) is the most prevalent opportunistic pathogenic fungus in the oral cavity, and Candida infection is considered as one of its high‐risk factors. Although oral microbiota–host interactions are closely associated with the development of OSCC, the interrelationship between fungi and OSCC is poorly understood compared to that between bacteria and viruses.ResultsWe accumulated knowledge of the evidence, pathogenic factors, and possible multiple mechanisms by which C. albicans promotes malignant transformation of OSCC, focusing on the induction of epithelial damage, production of carcinogens, and regulation of the tumor microenvironment. In addition, we highlight the latest treatment strategies for Candida infection.ConclusionThis review provides a new perspective on the interrelationship between C. albicans and OSCC and contributes to the establishment of a systematic and reliable clinical treatment system for OSCC patients with C. albicans infection.

Insights into the oral microbiota in human systemic cancers

“…A conspicuous correlation between the capacity of oral candida to metabolize alcohol into acetaldehyde and the fostering of cancer development corroborates the potential involvement of C. albicans in the carcinogenic tapestry ( Alnuaimi et al, 2016 ). The main carcinogenic mechanism of OSCC caused by Candida albicans infection is through the Kirsten rat sarcoma virus oncogene homolog (KRAS) pathway and the E2 transcription factor (E2F) gene ( Yang et al, 2023 ). In addition, mutations in tumor suppressor and DNA repair genes (such as p16, RAR-β2, TIMP3, BRCA1, and ERCC1) may have significant impact on the carcinogenic process due to C. albicans infection ( Yang et al, 2023 ).…”

“…The main carcinogenic mechanism of OSCC caused by Candida albicans infection is through the Kirsten rat sarcoma virus oncogene homolog (KRAS) pathway and the E2 transcription factor (E2F) gene ( Yang et al, 2023 ). In addition, mutations in tumor suppressor and DNA repair genes (such as p16, RAR-β2, TIMP3, BRCA1, and ERCC1) may have significant impact on the carcinogenic process due to C. albicans infection ( Yang et al, 2023 ). Published studies have described the association between fungal communities and tumor transformation, and demonstrated a decrease in the diversity of individual fungal species that make up the oral fungal community in patients with oral squamous cell carcinoma.…”

Fungal footprints in oral cancer: unveiling the oral mycobiome

“…Earlier studies have illuminated the interplay between distinct microbial communities, implying that these joint communities contribute to dysbiosis or the preservation of a healthy microbiome ( 72 ). While there is a range of data on the role of Candida in oral carcinogenesis ( 37 , 41 , 114 ), other species such as Aspergillus , Penicillium , and Malassezzia require additional investigation ( Figure 4 ). Overall, the study of the oral mycobiome is still in its infancy, and further research aiming at exploring the potential role of fungi in tuning and modulating the host immunity is essential to open up new possibilities for the prevention and adjunctive treatment of oral cancer.…”