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Autophagy mediates oral submucous fibrosis
Author(s) -
Li Jiang,
Tingting Zhao,
Peng Zhang,
ChaoJin Xu,
ZHUO-XIANG RONG,
ZI-YI YAN,
Changyun Fang
Publication year - 2016
Publication title -
experimental and therapeutic medicine
Language(s) - English
Resource type - Journals
eISSN - 1792-1015
pISSN - 1792-0981
DOI - 10.3892/etm.2016.3145
Subject(s) - oral submucous fibrosis , autophagy , fibroblast , fibrosis , apoptosis , biology , cancer research , transforming growth factor , signal transduction , microbiology and biotechnology , pathology , medicine , in vitro , biochemistry
Oral submucous fibrosis (OSF) is a chronic insidious disease of the oral mucosa, well-recognized as a premalignant condition and commonly found in Southern China. It is primarily caused by the habit of areca nut or gutkha chewing. OSF is believed to be a homeostatic disorder of the extracellular matrix and fibroblast proliferation. The present study demonstrated a novel link between autophagy and OSF. Tissue samples from human OSF showed an overexpression of the autophagy marker microtubule-associated protein 1 light chain 3 using immunohistochemistry and quantitative polymerase chain reaction. With regard to the crucial role of transforming growth factor (TGF)-β in OSF disease, western blot analysis demonstrated that TGF-β signaling was shown to contribute to the activation of autophagy in fibroblasts in vitro ; however, a cell apoptosis and MTS assay demonstrated that the suppression of autophagy ameliorated the fibrosis induced by active TGF-β receptor type I signaling, as well as promoted fibroblast apoptosis and suppressed proliferation. Therefore, the present results suggest that autophagy serves a crucial function in OSF.

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