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Objective: In this article, we review the current studies on the role of podoplanin in oral cancer and the potential application of podoplanin inhibitors as a therapeutic agent for oral cancer., Design: The narrative review approach was conducted, providing a comprehensive perspective of related literature. Publications addressing podoplanin and its inhibitors in the context of oral cancer were retrieved from PubMed and Scopus databases., Results: Podoplanin has emerged as a biomarker and therapeutic agent for oral cancer. Numerous studies have reported high podoplanin expression in oral cancer and pre-cancerous lesions compared to normal cells. A specific inhibitor targeting podoplanin may have the potential to prevent oral carcinogenesis via interfering with the pathway of cancerous cells involved in cell proliferation and metastasis. Antibodies, chimeric antigen receptor (CAR)-T cells, cancer-specific mAb (CasMab), synthetic molecules, and lectins are among the materials used as anticancer agents targeting podoplanin. Plant-derived lectins appear to demonstrate a unique advantage against alternative candidates., Conclusions: The use of podoplanin inhibitors in place of existing therapeutic approaches could be a promising and novel approach to the prevention and treatment of oral cancer. Nevertheless, further research is required to investigate the practical application of such inhibitors., Competing Interests: Declaration of Competing Interest The authors have no relevant financial or non-financial interests to disclose., (Copyright © 2023 Elsevier Ltd. All rights reserved.)

Oral carcinogenesis is preceded by oral diseases associated with inflammation such as periodontitis and oral candidiasis, which are contributed by chronic alcoholism, smoking, poor oral hygiene, and microbial infections. Dysbiosis is an imbalance of microbial composition due to oral infection, which has been reported to contribute to oral carcinogenesis. Therefore, in this review, we summarised the role of probiotics, prebiotics, synbiotics, and postbiotics in promoting a balanced oral microbiome, which may prevent oral carcinogenesis due to oral infections. Probiotics have been shown to produce biofilm, which possesses antibacterial activity against oral pathogens. Meanwhile, prebiotics can support growth and increase the benefit of probiotics. In addition, postbiotics possess antibacterial, anticariogenic, and anticancer properties that potentially aid in oral cancer prevention and treatment. The use of probiotics, prebiotics, synbiotics, and postbiotics for oral cancer management is still limited despite their vast potential, thus, discovering their prospects could herald a novel approach to disease prevention and treatment while participating in combating antimicrobial resistance., (© 2022. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.)

Objectives: This systematic review aimed to investigate the effects if probiotics can inhibit oral carcinogenesis., Design: PubMed, Web of Science, Scopus, and PLOS databases were searched up to February 2020 to identify randomised controlled trials that fulfilled the eligibility criteria. Joanna Briggs Institute (JBI) Critical Appraisal Tool was used for quality assessment of articles. This review was performed according to the Preferred Reporting Items for Systematic Review and Meta-analysis (PRISMA-P) 2015 protocol guidelines., Result: The initial search retrieved 774 articles. Of these, only five articles were included in the qualitative synthesis. Two out of the five papers were further analysed for quantitative synthesis in meta-analysis. The majority of the included studies were found to be of "moderate quality". The qualitative synthesis found four probiotics that exhibited potential therapeutic effects in oral carcinogenesis, includingAcetobacter syzygii, AJ2, Lactobacillus plantarum, and Lactobacillus salivarius REN. Among them, the application of L. salivarius REN resulted in a 95 % lower risk for developing oral cancer (p < 0.05)., Conclusion: It is known that probiotics have the potential to inhibit oral carcinogenesis, thus supporting the hypothesis of the study. The ability of L. salivarius REN to inhibit the development of oral cancer suggested that this bacterium can be a potential inhibitory agent against oral carcinogenesis., (Copyright © 2020 Elsevier Ltd. All rights reserved.)

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., (© 2020 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.)

Microbial infection has been shown to involve in oral carcinogenesis; however, the underlying mechanisms remain poorly understood. The present study aimed to characterize the growth of oral microorganisms as both monospecies and polymicrobial biofilms and determine the effects of their products on oral keratinocytes. Candida albicans (ALC3), Actinomyces naeslundii (AN) and Streptococcus mutans (SM) biofilms or a combination of these (TRI) were grown in flow-cell system for 24 h. The biofilms were subjected to fluorescent in situ hybridization using species-specific probes and analysed using confocal laser scanning microscopy. The effluent derived from each biofilm was collected and incubated with malignant (H357) and normal (OKF6) oral keratinocytes to assess extracellular matrix adhesion, epithelial-mesenchymal transition (EMT) and cytokines expression. Incubation of OKF6 with ALC3 and TRI effluent significantly decreased adhesion of the oral keratinocyte to collagen I, whereas incubation of H357 with similar effluent increased adhesion of the oral keratinocyte to laminin I, significantly when compared with incubation with artificial saliva containing serum-free medium (NE; P < 0.05). In OKF6, changes in E-cadherin and vimentin expression were not consistent with EMT although there was evidence of a mesenchymal to epithelial transition in malignant oral keratinocytes incubated with AN and SM effluent. A significant increase of pro-inflammatory cytokines expression, particularly interleukin (IL)-6 and IL-8, was observed when H357 was incubated with all biofilm effluents after 2- and 24-h incubation when compared with NE (P < 0.05). In conclusion, C.albicans, A.naeslundii and S.mutans form polymicrobial biofilms which differentially modulate malignant phenotype of oral keratinocytes., (© The Author(s) 2018. Published by Oxford University Press. All rights reserved. For Permissions, please email: journals.permissions@oup.com.)