<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Liao YW</submitter><funding>Ministry of Science and Technology</funding><pagination>4130-4138</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC6111815</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>22(9)</volume><pubmed_abstract>Oral submucous fibrosis (OSF) is a progressive scarring disease. MicroRNA-200b (miR-200b) has been reported as a tumour suppressor, but its role in the precancerous OSF remains unknown. In this study, we investigated the impact of miR-200b on myofibroblastic differentiation activity. Arecoline is a major areca nut alkaloid and has been employed to induce the elevated myofibroblast activity in human buccal mucosal fibroblasts (BMFs). Treatment of arecoline in BMFs dose-dependently reduced gene expression of miR-200b, which corresponded with the decreased expression of miR-200b in fBMFs. The arecoline-induced myofibroblast activities were abolished by overexpression of miR-200b in BMFs, and the same results were observed in fBMFs. In addition, α-SMA was inhibited by an increase in miR-200b. We further demonstrated that miR-200b-mediated decrease in ZEB2 led to down-regulation of α-SMA, vimentin. Loss of miR-200b resulted in enhanced collagen contraction and migration capabilities, and knockdown of ZEB2 reversed these phenomena. Lastly, we showed the expression of miR-200b was significantly less and ZEB2 was markedly higher in OSF tissues. These results suggested that down-regulation of miR-200b may contribute to the pathogenesis of areca quid-associated OSF through the regulation of ZEB2 and myofibroblast hallmarks.</pubmed_abstract><journal>Journal of cellular and molecular medicine</journal><pubmed_title>miR-200b ameliorates myofibroblast transdifferentiation in precancerous oral submucous fibrosis through targeting ZEB2.</pubmed_title><pmcid>PMC6111815</pmcid><funding_grant_id>MOST‐103‐2314‐B‐040 ‐016 ‐MY3</funding_grant_id><pubmed_authors>Liao YW</pubmed_authors><pubmed_authors>Hsieh PL</pubmed_authors><pubmed_authors>Yu CC</pubmed_authors><pubmed_authors>Chang YC</pubmed_authors></additional><is_claimable>false</is_claimable><name>miR-200b ameliorates myofibroblast transdifferentiation in precancerous oral submucous fibrosis through targeting ZEB2.</name><description>Oral submucous fibrosis (OSF) is a progressive scarring disease. MicroRNA-200b (miR-200b) has been reported as a tumour suppressor, but its role in the precancerous OSF remains unknown. In this study, we investigated the impact of miR-200b on myofibroblastic differentiation activity. Arecoline is a major areca nut alkaloid and has been employed to induce the elevated myofibroblast activity in human buccal mucosal fibroblasts (BMFs). Treatment of arecoline in BMFs dose-dependently reduced gene expression of miR-200b, which corresponded with the decreased expression of miR-200b in fBMFs. The arecoline-induced myofibroblast activities were abolished by overexpression of miR-200b in BMFs, and the same results were observed in fBMFs. In addition, α-SMA was inhibited by an increase in miR-200b. We further demonstrated that miR-200b-mediated decrease in ZEB2 led to down-regulation of α-SMA, vimentin. Loss of miR-200b resulted in enhanced collagen contraction and migration capabilities, and knockdown of ZEB2 reversed these phenomena. Lastly, we showed the expression of miR-200b was significantly less and ZEB2 was markedly higher in OSF tissues. These results suggested that down-regulation of miR-200b may contribute to the pathogenesis of areca quid-associated OSF through the regulation of ZEB2 and myofibroblast hallmarks.</description><dates><release>2018-01-01T00:00:00Z</release><publication>2018 Sep</publication><modification>2026-06-08T04:19:05.795Z</modification><creation>2026-06-08T03:14:31.408Z</creation></dates><accession>S-EPMC6111815</accession><cross_references><pubmed>29893466</pubmed><doi>10.1111/jcmm.13690</doi></cross_references></HashMap>