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Proliferative ability and accumulation of cancer stem cells in oral submucous fibrosis epithelium
Author(s) -
Xie Changqing,
Feng Hui,
Zhong Liang,
Shi Yujie,
Wei Zihao,
Hua Yufei,
Ji Ning,
Li Jing,
Tang Zhangui,
Chen Qianming
Publication year - 2020
Publication title -
oral diseases
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.953
H-Index - 87
eISSN - 1601-0825
pISSN - 1354-523X
DOI - 10.1111/odi.13347
Subject(s) - sox2 , epithelial dysplasia , pathology , immunohistochemistry , dysplasia , carcinogenesis , epithelium , oral submucous fibrosis , malignant transformation , atrophy , cancer , medicine , fibrosis , epithelial–mesenchymal transition , stem cell , cancer research , biology , metastasis , transcription factor , biochemistry , genetics , gene
Objectives The driving force of the malignant transformation of epithelial cells during oral submucous fibrosis (OSF) is an unsettled debate. We hypothesized that the expression and accumulation of cancer stem cells (CSCs) are accompanied by epithelial atrophy in OSF. Materials and Methods The expression levels of Ki67 (proliferation marker), SOX2, and Bmi1 (CSC marker) in the epithelium during the early, middle, and late stages of OSF were measured by immunohistochemistry. At the same time, we focused on the expression of three proteins in OSF patients with benign hyperkeratosis and epithelial dysplasia. Results The clinical cohort study showed upregulated expression of the proliferation‐associated protein Ki67 in atrophic epithelium in patients with OSF. The expression levels of SOX2 and Bmi1 showed an increasing trend in the progression of OSF. Ki67, SOX2, and Bmi1 were highly expressed in OSF tissues with dysplasia. Moreover, the three proteins were located at the epithelial and mesenchymal junctions, and their expression showed a positive correlation with each other. Conclusion The results suggest that CSC accumulation could be accompanied by epithelial atrophy during OSF, which may be responsible for the driving forces for OSF carcinogenesis.