Hinokitiol ablates myofibroblast activation in precancerous oral submucous fibrosis by targeting Snail

Hinokitiol ablates myofibroblast activation in precancerous oral submucous fibrosis by targeting... Oral submucous fibrosis (OSF) is a precancerous condition with symptoms of limited mouth opening and areca nut chewing habit has been implicated in its pathogenesis. Hinokitiol, a natural tropolone derived from Chamacyparis taiwanensis, has been reported to improve oral lichen planus and inhibit various cancer cells. Here, we showed that hinokitiol reduced the myofibroblast activities in fBMFs and prevented the arecoline‐induced transdifferentiation. Treatment of hinokitiol dose‐dependently downregulated the myofibroblast markers as well as various EMT transcriptional factors. In particular, we identified that Snail was able to bind to the E‐box in the α‐SMA promoter. Our data suggested that exposure of fBMFs to hinokitiol mitigated the hallmarks of myofibroblasts, while overexpression of Snail eliminated the effect of hinokitiol. These findings revealed that the inhibitory effect of hinokitiol on myofibroblasts was mediated by repression of α‐SMA via regulation of Snail and showed the anti‐fibrotic potential of hinokitiol in the treatment of OSF. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Environmental Toxicology Wiley

Hinokitiol ablates myofibroblast activation in precancerous oral submucous fibrosis by targeting Snail

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Publisher
Wiley
Copyright
© 2018 Wiley Periodicals, Inc.
ISSN
1520-4081
eISSN
1522-7278
D.O.I.
10.1002/tox.22531
Publisher site
See Article on Publisher Site

Abstract

Oral submucous fibrosis (OSF) is a precancerous condition with symptoms of limited mouth opening and areca nut chewing habit has been implicated in its pathogenesis. Hinokitiol, a natural tropolone derived from Chamacyparis taiwanensis, has been reported to improve oral lichen planus and inhibit various cancer cells. Here, we showed that hinokitiol reduced the myofibroblast activities in fBMFs and prevented the arecoline‐induced transdifferentiation. Treatment of hinokitiol dose‐dependently downregulated the myofibroblast markers as well as various EMT transcriptional factors. In particular, we identified that Snail was able to bind to the E‐box in the α‐SMA promoter. Our data suggested that exposure of fBMFs to hinokitiol mitigated the hallmarks of myofibroblasts, while overexpression of Snail eliminated the effect of hinokitiol. These findings revealed that the inhibitory effect of hinokitiol on myofibroblasts was mediated by repression of α‐SMA via regulation of Snail and showed the anti‐fibrotic potential of hinokitiol in the treatment of OSF.

Journal

Environmental ToxicologyWiley

Published: Jan 1, 2018

Keywords: ; ; ; ;

References

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