Int J Stomatol

Int J Stomatol ›› 2019, Vol. 46 ›› Issue (6): 705-710.doi: 10.7518/gjkq.2019104

• Reviews • Previous Articles     Next Articles

Research progress on the mechanism of Candida albicans in oral carcinogenesis

Wen Shuqiong,Guo Junyi,Dai Wenxiao,Wang Dikan,Wang Zhi()   

  1. Guanghua School of Stomatology, Dept. of Oral Medicine, Hospital of Stomatology, Sun Yat-sen University, Guangdong Provincial Key Laboratory of Stomatology, Guangzhou 510055, China
  • Received:2019-02-24 Revised:2019-05-16 Online:2019-11-01 Published:2019-11-14
  • Contact: Zhi Wang E-mail:wangzh75@sysu.edu.cn
  • Supported by:
    This study was supported by National Natural Science Foundation of China(81772896)

RichHTML

17

PDF (PC)

568

Abstract:

Microbial infection is one of the important causes of carcinogenesis. To date, an increasing number of researches have indicated that Candida albicans can increase the patients’ risk of carcinogenesis and tumor metastasis through the immunosuppressive state. Recent studies have demonstrated that Candida albicans promote the carcinogenesis through several mechanisms such as producing carcinogenic byproducts, triggering inflammation and inducing T helper cell 17 response. Here, we provide an overview of the research progress of oncogenic potential of Candida albicans and discuss the relationship between Candida albicans and cancer, trying to provide new ideas for the prevention and treatment of oral cancer.

Key words: Candida albicans, carcinogen, carcinogenesis, inflammation, T helper cell 17 immune response

CLC Number: 

  • R781.5 +4

TrendMD: 

Fig 1

Candida albicans invades oral epithelial cells"

Fig 2

Candida albicans promotes oral cancer through chronic inflammation"

[1] McManus BA, Coleman DC . Molecular epidemiology, phylogeny and evolution of Candida albicans[J]. Infect Genet Evol, 2014,21:166-178.
[2] Barrett AW, Kingsmill VJ, Speight PM . The frequency of fungal infection in biopsies of oral mucosal lesions[J]. Oral Dis, 1998,4(1):26-31.
[3] Roed-Petersen B, Renstrup G, Pindborg JJ . Candida in oral leukoplakias. A histologic and exfoliative cytologic study[J]. Scand J Dent Res, 1970,78(4):323-328.
[4] O’Grady JF, Reade PC . Candida albicans as a promoter of oral mucosal neoplasia[J]. Carcinogenesis, 1992,13(5):783-786.
[5] 章魁华, 王洪君, 秦锦霞 , 等. 白色念珠菌感染对增生口腔粘膜上皮的影响[J]. 中华口腔医学杂志, 1994,29(6):339-341, 384.
Zhang KH, Wang HJ, Qin JX , et al. Effect of candidal infection on the hyperplastic oral epithelium[J]. Chin J Stomatol, 1994,29(6):339-341, 384.
[6] Naglik JR, König A, Hube B , et al. Candida albicans-epithelial interactions and induction of mucosal innate immunity[J]. Curr Opin Microbiol, 2017,40:104-112.
[7] Ho J, Yang X, Nikou SA , et al. Candidalysin activates innate epithelial immune responses via epidermal growth factor receptor[J]. Nat Commun, 2019,10(1):2297.
[8] Filler SG . Candida-host cell receptor-ligand interactions[J]. Curr Opin Microbiol, 2006,9(4):333-339.
[9] Wächtler B, Citiulo F, Jablonowski N , et al. Candida albicans-epithelial interactions: dissecting the roles of active penetration, induced endocytosis and host factors on the infection process[J]. PLoS One, 2012,7(5):e36952.
[10] Allert S, Förster TM, Svensson CM , et al. Candida albicans-induced epithelial damage mediates translocation through intestinal barriers[J]. MBio, 2018,9(3):e00915-e00918.
[11] Naglik JR, Moyes DL, Wächtler B , et al. Candida albicans interactions with epithelial cells and mucosal immunity[J]. Microbes Infect, 2011,13(12/13):963-976.
[12] Hornbach A, Heyken A, Schild L , et al. The glycosylphosphatidylinositol-anchored protease Sap9 modulates the interaction of Candida albicans with human neutrophils[J]. Infect Immun, 2009,77(12):5216-5224.
[13] Furlaneto MC, Favero D, França EJ , et al. Effects of human blood red cells on the haemolytic capability of clinical isolates of Candida tropicalis[J]. J Biomed Sci, 2015,22:13.
[14] Tao L, Du H, Guan G , et al. Discovery of a “white-gray-opaque” tristable phenotypic switching system in Candida albicans: roles of non-genetic diversity in host adaptation[J]. PLoS Biol, 2014,12(4):e1001830.
[15] Zhu W, Filler SG . Interactions of Candida albicans with epithelial cells[J]. Cell Microbiol, 2010,12(3):273-282.
[16] Noble SM, Gianetti BA, Witchley JN . Candida albicans cell-type switching and functional plasticity in the mammalian host[J]. Nat Rev Microbiol, 2017,15(2):96-108.
[17] Krogh P . The role of yeasts in oral cancer by means of endogenous nitrosation[J]. Acta Odontol Scand, 1990,48(1):85-88.
[18] Sanjaya PR, Gokul S, Gururaj Patil B , et al. Candida in oral pre-cancer and oral cancer[J]. Med Hypotheses, 2011,77(6):1125-1128.
[19] Seitz HK, Cho CH . Contribution of alcohol and tobacco use in gastrointestinal cancer development[J]. Methods Mol Biol, 2009,472:217-241.
[20] Seitz HK, Stickel F . Molecular mechanisms of alcohol-mediated carcinogenesis[J]. Nat Rev Cancer, 2007,7(8):599-612.
[21] Hooper SJ, Wilson MJ, Crean SJ . Exploring the link between microorganisms and oral cancer: a systematic review of the literature[J]. Head Neck, 2009,31(9):1228-1239.
[22] Tsai ST, Wong TY, Ou CY , et al. The interplay between alcohol consumption, oral hygiene, ALDH2 and ADH1B in the risk of head and neck cancer[J]. Int J Cancer, 2014,135(10):2424-2436.
[23] Alnuaimi AD, Ramdzan AN, Wiesenfeld D , et al. Candida virulence and ethanol-derived acetaldehyde production in oral cancer and non-cancer subjects[J]. Oral Dis, 2016,22(8):805-814.
[24] Bakri MM, Rich AM, Cannon RD , et al. In vitro expression of Candida albicans alcohol dehydrogenase genes involved in acetaldehyde metabolism[J]. Mol Oral Microbiol, 2015,30(1):27-38.
[25] Elinav E, Nowarski R, Thaiss CA , et al. Inflammation-induced cancer: crosstalk between tumours, immune cells and microorganisms[J]. Nat Rev Cancer, 2013,13(11):759-771.
[26] Garrett WS . Cancer and the microbiota[J]. Science, 2015,348(6230):80-86.
[27] Brennan CA, Garrett WS . Gut microbiota, inflammation, and colorectal cancer[J]. Annu Rev Microbiol, 2016,70:395-411.
[28] Sun Y, Liu N, Guan X , et al. Immunosuppression induced by chronic inflammation and the progression to oral squamous cell carcinoma[J]. Mediators Inflamm, 2016,2016:5715719.
[29] Nasry WHS, Rodriguez-Lecompte JC, Martin CK . Role of COX-2/PGE2 mediated inflammation in oral squamous cell carcinoma[J]. Cancers (Basel), 2018,10(10):E348.
[30] Sonis ST, Amaral Mendes R . Could the PI3K canonical pathway be a common link between chronic inflammatory conditions and oral carcinogenesis[J]. J Oral Pathol Med, 2016,45(7):469-474.
[31] Mantovani A, Allavena P, Sica A , et al. Cancer-related inflammation[J]. Nature, 2008,454(7203):436-444.
[32] Netea MG, Sutmuller R, Hermann C , et al. Toll-like receptor 2 suppresses immunity against Candida albicans through induction of IL-10 and regulatory T cells[J]. J Immunol, 2004,172(6):3712-3718.
[33] Drummond RA, Franco LM, Lionakis MS . Human CARD9: a critical molecule of fungal immune surveillance[J]. Front Immunol, 2018,9:1836.
[34] Terayama Y, Matsuura T, Ozaki K . Lack of correlation between aberrant p16, RAR-β2, TIMP3, ERCC1, and BRCA1 protein expression and promoter methylation in squamous cell carcinoma accompanying Candida albicans-induced inflammation[J]. PLoS One, 2016,11(7):e0159090.
[35] Feller L, Khammissa RA, Chandran R , et al. Oral candidosis in relation to oral immunity[J]. J Oral Pathol Med, 2014,43(8):563-569.
[36] Richardson JP, Moyes DL . Adaptive immune responses to Candida albicans infection[J]. Virulence, 2015,6(4):327-337.
[37] Netea MG, Joosten LA, van der Meer JW, et al. Immune defence against Candida fungal infections[J]. Nat Rev Immunol, 2015,15(10):630-642.
[38] Becker KL, Ifrim DC, Quintin J , et al. Antifungal innate immunity: recognition and inflammatory networks[J]. Semin Immunopathol, 2015,37(2):107-116.
[39] Tang J, Lin G, Langdon WY , et al. Regulation of C- type lectin receptor-mediated antifungal immunity[J]. Front Immunol, 2018,9:123.
[40] Dennehy KM, Willment JA, Williams DL , et al. Reciprocal regulation of IL-23 and IL-12 following co- activation of Dectin-1 and TLR signaling pathways[J]. Eur J Immunol, 2009,39(5):1379-1386.
[41] Rodríguez M, Márquez S, de la Rosa JV, et al. Fungal pattern receptors down-regulate the inflammatory response by a cross-inhibitory mechanism independent of interleukin-10 production[J]. Immunology, 2017,150(2):184-198.
[42] Mengesha BG, Conti HR . The role of IL-17 in protection against mucosal Candida infections[J]. J Fungi (Basel), 2017,3(4):E52.
[43] Kirchner FR, Littringer K, Altmeier S , et al. Persistence of Candida albicans in the oral mucosa induces a curbed inflammatory host response that is independent of immunosuppression[J]. Front Immunol, 2019,10:330.
[44] Amatya N, Garg AV, Gaffen SL . IL-17 signaling: the yin and the yang[J]. Trends Immunol, 2017,38(5):310-322.
[45] Martínez-López M, Iborra S, Conde-Garrosa R , et al. Microbiota sensing by mincle-syk axis in dendritic cells regulates interleukin-17 and -22 production and promotes intestinal barrier integrity[J]. Immunity, 2019,50(2): 446-461.e9.
[46] Uribe-Querol E, Rosales C . Neutrophils in cancer: two sides of the same coin[J]. J Immunol Res, 2015,2015:983698.
[47] Magalhaes MA, Glogauer JE, Glogauer M . Neutrophils and oral squamous cell carcinoma: lessons learned and future directions[J]. J Leukoc Biol, 2014,96(5):695-702.
[48] Langowski JL, Zhang X, Wu L , et al. IL-23 promotes tumour incidence and growth[J]. Nature, 2006,442(7101):461-465.
[1] Abulaiti Guliqihere,Qin Xu,Zhu Guangxun. Research progress of mitophagy in the onset and development of periodontal disease [J]. Int J Stomatol, 2024, 51(1): 68-73.
[2] Gong Meiling,Cheng Xingqun,Wu Hongkun.. Research progress on the correlation between Parkinson’s disease and periodontitis [J]. Int J Stomatol, 2023, 50(5): 587-593.
[3] Yang Xiaoyu,Yuan Quan.. Research progress on the role of extravascular fibrinogen deposition in mucosal diseases [J]. Int J Stomatol, 2023, 50(4): 457-462.
[4] Huang Dingming, Zhang Lan, Man Yi. Biologic bases of nature tooth-related maxillary sinus floor elevation [J]. Int J Stomatol, 2023, 50(3): 251-262.
[5] Sun Jia,Han Ye,Hou Jianxia. Research progress on the role of interleukin-6-hepcidin signal axis in regulating the pathogenesis of periodontitis-associated anemia [J]. Int J Stomatol, 2023, 50(3): 329-334.
[6] Liu Yi,Liu Yi.. Research progress on the regulation of bone remodeling by macrophage-derived exosomes [J]. Int J Stomatol, 2023, 50(1): 120-126.
[7] Liu Tiqian,Liang Xing,Liu Weiqing,Li Xiaohong,Zhu Rui.. Research progress on the role and mechanism of occlusal trauma in the development of periodontitis [J]. Int J Stomatol, 2023, 50(1): 19-24.
[8] Yang Sirui,Ren Biao,Peng Xian,Xu Xin. Research progress on drug synergism with fluconazole in fluconazole-resistant Candida albicans [J]. Int J Stomatol, 2022, 49(5): 511-520.
[9] Li Shanshan,Yang Fang. Research progress on the relationship between Streptococcus mutans and Candida albicans in caries [J]. Int J Stomatol, 2022, 49(4): 392-396.
[10] Liu Qianxi,Wu Jiayi,Ren Biao,Huang Ruijie. Research progress on the interactions between Enterococcus faecalis and other oral microorganisms [J]. Int J Stomatol, 2022, 49(3): 290-295.
[11] Li Guiping,Qin Xu,Zhu Guangxun.. Research progress on adenosine monophosphate-activated protein kinase in periodontal disease [J]. Int J Stomatol, 2022, 49(3): 343-348.
[12] Jiang Duan,Shen Daonan,Zhao Lei,Wu Yafei. Research progress on the relationship between new anti-inflammatory factor developmental endothelial locus-1 and periodontitis [J]. Int J Stomatol, 2022, 49(2): 244-248.
[13] Zhou Yi,Zhao Yuming. Research progress on various dental pulp regeneration scaffolds [J]. Int J Stomatol, 2022, 49(1): 19-26.
[14] Liu Jiacheng,Meng Zhaosong,Li Hongjie,Sui Lei. The role of follistatin in oral and maxillofacial development and its therapeutic application prospect [J]. Int J Stomatol, 2021, 48(5): 556-562.
[15] Zhou Feng,Chen Ye,Chen Chen,Zhang Yining,Geng Ruiman,Liu Ji. Mechanism of sirtuin 1 in regulating periodontitis [J]. Int J Stomatol, 2021, 48(3): 341-346.
Viewed
Full text


Abstract

Cited
  Shared   
  Discussed   
[1] . [J]. Foreign Med Sci: Stomatol, 1999, 26(06): .
[2] . [J]. Foreign Med Sci: Stomatol, 1999, 26(06): .
[3] . [J]. Foreign Med Sci: Stomatol, 1999, 26(06): .
[4] . [J]. Foreign Med Sci: Stomatol, 1999, 26(06): .
[5] . [J]. Foreign Med Sci: Stomatol, 1999, 26(05): .
[6] . [J]. Foreign Med Sci: Stomatol, 1999, 26(05): .
[7] . [J]. Foreign Med Sci: Stomatol, 1999, 26(04): .
[8] . [J]. Foreign Med Sci: Stomatol, 1999, 26(04): .
[9] . [J]. Foreign Med Sci: Stomatol, 2004, 31(02): 126 -128 .
[10] . [J]. Inter J Stomatol, 2008, 35(S1): .