口腔黏膜下纤维化恶变的研究进展

doi:10.3760/cma.j.cn371439-20220609-00120

国际肿瘤学杂志 ›› 2022, Vol. 49 ›› Issue (10): 608-611.doi: 10.3760/cma.j.cn371439-20220609-00120

口腔黏膜下纤维化恶变的研究进展

周昌群¹, 管晓燕^1,², 刘建国², 岳超弈³, 廖成成^1,²()

¹遵义医科大学附属口腔医院正畸科二组，遵义 563000
²贵州省普通高等学校口腔疾病研究特色重点实验室，遵义 563000
³遵义医科大学医学与科技学院，遵义 563000

收稿日期:2022-06-09 修回日期:2022-06-18 出版日期:2022-10-08 发布日期:2022-12-01
通讯作者: 廖成成 E-mail:lcc_950330@163.com
基金资助:
国家重点研发计划(2016YFC1102800);国家自然科学基金(82060205);贵州省医用生物材料研发人才基地(Qianren Lingfa [2018] No. 3）);贵州省普通高等学校青年科技人才成长项目(Qianjiao He KY Word [2021] 215)

Research progress on the malignant transformation of oral submucosal fibrosis

Zhou Changqun¹, Guan Xiaoyan^1,², Liu Jianguo², Yue Chaoyi³, Liao Chengcheng^1,²()

¹Group 2， Department of Orthodontics， Affiliated Stomatological Hospital of Zunyi Medical University， Zunyi 563000， China
²Key Laboratory of Oral Disease Research in General Colleges and Universities of Guizhou Province， Zunyi 563000， China
³School of Medicine and Technology， Zunyi Medical University， Zunyi 563000， China

Received:2022-06-09 Revised:2022-06-18 Online:2022-10-08 Published:2022-12-01
Contact: Liao Chengcheng E-mail:lcc_950330@163.com
Supported by:
National Key Research and Development Program Project of China(2016YFC1102800);National Natural Science Foundation of China(82060205);Guizhou Province Medical Biomaterials Research and Development Talent Base Project(Qianren Lingfa [2018] No. 3）);Growth Project(Qianjiao He KY Word [2021] 215)

摘要/Abstract

摘要：

口腔黏膜下纤维化（OSF）可引起患者各种口腔功能障碍，并可恶变为口腔癌。OSF恶变的原因及过程涉及咀嚼槟榔、血管萎缩、组织缺氧、细胞周期改变、衰老、自噬、癌/抑癌基因、微小RNA改变等方面。研究OSF恶变原因及过程对OSF治疗、预防其恶变有重要意义。

关键词: 口腔黏膜下纤维化, 口腔肿瘤, 恶变

Abstract:

Oral submucous fibrosis （OSF） can cause various oral dysfunctions in patients and can turn into oral cancer. The causes and processes of OSF malignant transformation involve betel nut chewing， vascular atrophy， tissue hypoxia， cell cycle changes， aging， autophagy， and changes in cancer/cancer suppressor genes and microRNAs. It is of great significance to study the causes and process of OSF malignant transformation for the treatment and prevention of OSF malignant transformation.

Key words: Oral submucous fibrosis, Oral neoplasms, Malignant change

周昌群, 管晓燕, 刘建国, 岳超弈, 廖成成. 口腔黏膜下纤维化恶变的研究进展[J]. 国际肿瘤学杂志, 2022, 49(10): 608-611.

Zhou Changqun, Guan Xiaoyan, Liu Jianguo, Yue Chaoyi, Liao Chengcheng. Research progress on the malignant transformation of oral submucosal fibrosis[J]. Journal of International Oncology, 2022, 49(10): 608-611.

参考文献 39

[1]	Mello FW, Miguel AFP, Dutra KL, et al. Prevalence of oral potentially malignant disorders: a systematic review and meta-analysis[J]. J Oral Pathol Med, 2018, 47(7): 633-640. DOI: 10.1111/jop.12726. doi: 10.1111/jop.12726 pmid: 29738071
[2]	Shih YH, Wang TH, Shieh TM, et al. Oral submucous fibrosis: a review on etiopathogenesis, diagnosis, and therapy[J]. Int J Mol Sci, 2019, 20(12): 2940. DOI: 10.3390/ijms20122940. doi: 10.3390/ijms20122940
[3]	Wu YH, Lin PY, Yang JH, et al. Significantly higher serum tumor marker levels in patients with oral submucous fibrosis[J]. J Dent Sci, 2021, 16(3): 846-853. DOI: 10.1016/j.jds.2021.02.009. doi: 10.1016/j.jds.2021.02.009
[4]	Oliveira NG, Ramos DL, Dinis-Oliveira RJ. Genetic toxicology and toxicokinetics of arecoline and related areca nut compounds: an updated review[J]. Arch Toxicol, 2021, 95(2): 375-393. DOI: 10.1007/s00204-020-02926-9. doi: 10.1007/s00204-020-02926-9 pmid: 33097969
[5]	Islam S, Uehara O, Matsuoka H, et al. DNA hypermethylation of sirtuin 1 (SIRT1) caused by betel quid chewing—a possible predictive biomarker for malignant transformation[J]. Clin Epigenetics, 2020, 12(1): 12. DOI: 10.1186/s13148-019-0806-y. doi: 10.1186/s13148-019-0806-y
[6]	Yao M, Li J, Yuan S, et al. Role of the arecoline/YAP1/BMP4 pathway in promoting endothelial-mesenchymal transition in oral submucous fibrosis[J]. J Oral Pathol Med, 2020, 49(4): 305-310. DOI: 10.1111/jop.12945. doi: 10.1111/jop.12945 pmid: 31397922
[7]	Zheng L, Guan ZJ, Pan WT, et al. Tanshinone suppresses arecoline-induced epithelial-mesenchymal transition in oral submucous fibrosis by epigenetically reactivating the p53 pathway[J]. Oncol Res, 2018, 26(3): 483-494. DOI: 10.3727/096504017X14941825760362. doi: 10.3727/096504017X14941825760362 pmid: 28550687
[8]	Chen SY, Chang YL, Liu ST, et al. Differential cytotoxicity mechanisms of copper complexed with disulfiram in oral cancer cells[J]. Int J Mol Sci, 2021, 22(7): 3711. DOI: 10.3390/ijms22073711. doi: 10.3390/ijms22073711
[9]	Tekade SA, Chaudhary MS, Tekade SS, et al. Early stage oral submucous fibrosis is characterized by increased vascularity as opposed to advanced stages[J]. J Clin Diagn Res, 2017, 11(5): ZC92-ZC96. DOI: 10.7860/JCDR/2017/25800.9948. doi: 10.7860/JCDR/2017/25800.9948
[10]	Pammar C, Nayak RS, Kotrashetti VS, et al. Comparison of microvessel density using CD34 and CD105 in oral submucous fibrosis and its correlation with clinicopathological features: an immunohistochemical study[J]. J Cancer Res Ther, 2018, 14(5): 983-988. DOI: 10.4103/0973-1482.181186. doi: 10.4103/0973-1482.181186 pmid: 30197335
[11]	Tom A, Baghirath V, Krishna B, et al. Ultrastructural changes of collagen in different histopathological grades of oral submucous fibrosis[J]. J Pharm Bioallied Sci, 2019, 11(Suppl 2): S309-S313. DOI: 10.4103/JPBS.JPBS_20_19. doi: 10.4103/JPBS.JPBS_20_19
[12]	Rashid M, Zadeh LR, Baradaran B, et al. Up-down regulation of HIF-1α in cancer progression[J]. Gene, 2021, 798: 145796. DOI: 10.1016/j.gene.2021.145796. doi: 10.1016/j.gene.2021.145796
[13]	Cheng RH, Wang YP, Chang JY, et al. Genetic susceptibility and protein expression of extracellular matrix turnover-related genes in oral submucous fibrosis[J]. Int J Mol Sci, 2020, 21(21): 8104. DOI: 10.3390/ijms21218104. doi: 10.3390/ijms21218104
[14]	Anura A, Kazi A, Pal M, et al. Endorsing cellular competitiveness in aberrant epithelium of oral submucous fibrosis progression: neighbourhood analysis of immunohistochemical attributes[J]. Histochem Cell Biol, 2018, 150(1): 61-75. DOI: 10.1007/s00418-018-1671-z. doi: 10.1007/s00418-018-1671-z pmid: 29687243
[15]	Zhang L, Tan J, Liu YP, et al. Curcumin relieves the arecoline-induced fibrosis of oral mucosal fibroblasts via inhibiting HIF-1α/TGF-β/CTGF signaling pathway: an in vitro study[J]. Toxicol Res (Camb), 2021, 10(3): 631-638. DOI: 10.1093/toxres/tfab046. doi: 10.1093/toxres/tfab046
[16]	Xie C, Feng H, Zhong L, et al. Proliferative ability and accumulation of cancer stem cells in oral submucous fibrosis epithelium[J]. Oral Dis. 2020, 26(6): 1255-1264. DOI: 10.1111/odi.13347. doi: 10.1111/odi.13347
[17]	Patil S, Sarode SC, Ashi H, et al. Triphala extract negates arecoline-induced senescence in oral mucosal epithelial cells in vitro[J]. Saudi J Biol Sci, 2021, 28(4): 2223-2228. DOI: 10.1016/j.sjbs.2021.01.011. doi: 10.1016/j.sjbs.2021.01.011 pmid: 33911939
[18]	Nag R, Paul RR, Pal M, et al. Epithelial distribution of E-cadherin, p63, and mitotic figures in ApoTome images to determine the oncogenic potentiality of oral submucous fibrosis[J]. Microsc Microanal, 2020, 26(6): 1198-1210. DOI: 10.1017/S143192762 0024538. doi: 10.1017/S1431927620024538 pmid: 33050978
[19]	Birch J, Gil J. Senescence and the SASP: many therapeutic avenues[J]. Genes Dev, 2020, 34(23/24): 1565-1576. DOI: 10.1101/gad.343129.120. doi: 10.1101/gad.343129.120
[20]	Sharma M, Hunter KD, Fonseca FP, et al. Emerging role of cellular senescence in the pathogenesis of oral submucous fibrosis and its malignant transformation[J]. Head Neck, 2021, 43(10): 3153-3164. DOI: 10.1002/hed.26805. doi: 10.1002/hed.26805
[21]	Zhu B, Jiang Q, Que G, et al. Role of autophagy and apoptosis in atrophic epithelium in oral submucous fibrosis[J]. J Oral Sci, 2020, 62(2): 184-188. DOI: 10.2334/josnusd.19-0170. doi: 10.2334/josnusd.19-0170 pmid: 32132327
[22]	Wang J, Yang L, You J, et al. Platelet-derived growth factor regulates the biological behavior of oral mucosal fibroblasts by inducing cell autophagy and its mechanism[J]. J Inflamm Res, 2021, 14: 3405-3417. DOI: 10.2147/JIR.S313910. doi: 10.2147/JIR.S313910 pmid: 34305405
[23]	Dai Z, Zhu B, Yu H, et al. Role of autophagy induced by arecoline in angiogenesis of oral submucous fibrosis[J]. Arch Oral Biol, 2019, 102: 7-15. DOI: 10.1016/j.archoralbio.2019.03.021. doi: S0003-9969(19)30061-5 pmid: 30951892
[24]	Kumari P, Debta P, Dixit A. Oral potentially malignant disorders: etiology, pathogenesis, and transformation into oral cancer[J]. Front Pharmacol, 2022, 13: 825266. DOI: 10.3389/fphar.2022.825266. doi: 10.3389/fphar.2022.825266
[25]	Siriwardena BSMS, Jayawardena KLTD, Senarath NH, et al. An evaluation of clinical and histopathological aspects of patients with oral submucous fibrosis in the background of oral squamous cell carcinoma[J]. Biomed Res Int, 2018, 2018: 4154165. DOI: 10.1155/2018/4154165. doi: 10.1155/2018/4154165
[26]	Mukherjee S, Katarkar A, Dhariwal R, et al. Effect of lysyl oxidase G473 A polymorphism on lysyl oxidase and total soluble collagen expression in oral submucous fibrosis[J]. Asian Pac J Cancer Prev, 2021, 22(8): 2493-2499. DOI: 10.31557/APJCP.2021.22.8.2493. doi: 10.31557/APJCP.2021.22.8.2493
[27]	Monteiro R, Hallikeri K, Sudhakaran A. PTEN and α-SMA expression and diagnostic role in oral submucous fibrosis and oral squamous cell carcinoma with concomitant oral submucous fibrosis[J]. J Oral Maxillofac Res, 2021, 12(1): e3. DOI: 10.5037/jomr.2021.12103. doi: 10.5037/jomr.2021.12103
[28]	Zhou S, Zhu Y, He Z, et al. Long non-coding RNA expression profile associated with malignant progression of oral submucous fibrosis[J]. J Oncol, 2019, 2019: 6835176. DOI: 10.1155/2019/6835176. doi: 10.1155/2019/6835176
[29]	Kavitha L, Ranganathan K, Shyam S, et al. Immunohistochemical biomarkers in oral submucous fibrosis: a scoping review[J]. J Oral Pathol Med, 2022, 51(7): 594-602. DOI: 10.1111/jop.13280. doi: 10.1111/jop.13280
[30]	朱蓉, 翦新春, 刘德裕, 等. PTPRZ1在口腔黏膜下纤维性变癌变中的表达及临床意义[J]. 上海口腔医学, 2017, 26(2): 198-203. DOI: 10.19439/j.sjos.2017.02.015. doi: 10.19439/j.sjos.2017.02.015
[31]	Xia Z, Ouyang D, Li Q, et al. The expression, functions, interactions and prognostic values of PTPRZ1: a review and bioinformatic analysis[J]. J Cancer, 2019, 10(7): 1663-1674. DOI: 10.7150/jca.28231. doi: 10.7150/jca.28231 pmid: 31205522
[32]	Ma L, Shen T, Peng H, et al. Overexpression of PTPRZ1 regulates p120/β-catenin phosphorylation to promote carcinogenesis of oral submucous fibrosis[J]. J Oncol, 2022, 2022: 2352360. DOI: 10.1155/2022/2352360. doi: 10.1155/2022/2352360
[33]	Mao T, Xiong H, Hu X, et al. DEC1: a potential biomarker of malignant transformation in oral leukoplakia[J]. Braz Oral Res, 2020, 34: e052. DOI: 10.1590/1807-3107bor-2020.vol34.0052. doi: 10.1590/1807-3107bor-2020.vol34.0052 pmid: 32578762
[34]	Yang L, Zeng L, Wang Z, et al. Differentiated embryo chondrocyte 1, induced by hypoxia-inducible factor 1α, promotes cell migration in oral squamous cell carcinoma cell lines[J]. Oral Surg Oral Med Oral Pathol Oral Radiol, 2022, 133(2): 199-206. DOI: 10.1016/j.oooo.2021.08.022. doi: 10.1016/j.oooo.2021.08.022
[35]	Hu X, Wang W, Hu Y, et al. Overexpression of DEC1 in the epithelium of OSF promotes mesenchymal transition via activating FAK/Akt signal axis[J]. J Oral Pathol Med, 2022, 51(9): 780-790. DOI: 10.1111/jop.13350. doi: 10.1111/jop.13350
[36]	Jishnu PV, Shenoy SU, Sharma M, et al. Comprehensive analysis of microRNAs and their target genes in oral submucous fibrosis[J]. Oral Dis, 2022, In press. DOI: 10.1111/odi.14219. doi: 10.1111/odi.14219
[37]	Yang HW, Yu CC, Hsieh PL, et al. Arecoline enhances miR-21 to promote buccal mucosal fibroblasts activation[J]. J Formos Med Assoc, 2021, 120(4): 1108-1113. DOI: 10.1016/j.jfma.2020.10.019. doi: 10.1016/j.jfma.2020.10.019
[38]	Liao YW, Tsai LL, Lee YH, et al. miR-21 promotes the fibrotic properties in oral mucosa through targeting PDCD4[J]. J Dent Sci, 2022, 17(2): 677-682. DOI: 10.1016/j.jds.2021.09.004. doi: 10.1016/j.jds.2021.09.004
[39]	Chang C, Wang H, Liu J, et al. Porphyromonas gingivalis infection promoted the proliferation of oral squamous cell carcinoma cells through the miR-21/PDCD4/AP-1 negative signaling pathway[J]. ACS Infect Dis, 2019, 5(8): 1336-1347. DOI: 10.1021/acsinfecdis.9b00032. doi: 10.1021/acsinfecdis.9b00032 pmid: 31243990

口腔黏膜下纤维化恶变的研究进展

Research progress on the malignant transformation of oral submucosal fibrosis

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