Research Papers:

By inhibiting snail signaling and miR-23a-3p, osthole suppresses the EMT-mediated metastatic ability in prostate cancer

Yu-Ching Wen, Wei-Jiunn Lee, Peng Tan, Shun-Fa Yang, Michael Hsiao, Liang-Ming Lee and Ming-Hsien Chien _

PDF  |  HTML  |  Supplementary Files  |  How to cite

Oncotarget. 2015; 6:21120-21136. https://doi.org/10.18632/oncotarget.4229

Metrics: PDF 1970 views  |   HTML 3087 views  |   ?  


Yu-Ching Wen1,2, Wei-Jiunn Lee2, Peng Tan1, Shun-Fa Yang3,4, Michael Hsiao5, Liang-Ming Lee2 and Ming-Hsien Chien1,6

1 Graduate Institute of Clinical Medicine, College of Medicine, Taipei Medical University, Taipei, Taiwan

2 Department of Urology, Wan Fang Hospital, Taipei Medical University, Taipei, Taiwan

3 Institute of Medicine, Chung Shan Medical University, Taichung, Taiwan

4 Department of Medical Research, Chung Shan Medical University Hospital, Taichung, Taiwan

5 The Genomics Research Center, Academia Sinica; Taipei, Taiwan

6 Department of Education and Research, Wan Fang Hospital, Taipei Medical University, Taipei, Taiwan

Correspondence to:

Ming-Hsien Chien, email:

Liang-Ming Lee, email:

Keywords: prostate cancer, miR-23a-3p, snail, EMT, osthole

Received: March 12, 2015 Accepted: May 13, 2015 Published: May 22, 2015


Here we showed that Osthole, 7-methoxy-8-(3-methyl-2-butenyl) coumarin, a bioactive coumarin derivative extracted from medicinal plants, inhibited migration, invasion, epithelial to mesenchymal transition (EMT) in androgen-independent prostate cancer (AIPC) cells in vitro and metastasis of AIPC in vivo. In patients, high Snail levels were correlated with a higher histological Gleason sum and poor survival rates. Osthole inhibited the TGF-β/Akt/MAPK pathways, reduced Snail-DNA-binding activity and induced E-cadherin. We found that osthole decreased miR-23a-3p. Ectopic miR-23a-3p suppressed E-cadherin 3’ untranslated region reporter activity and E-cadherin expression, and relieved the motility suppression caused by osthole treatment.

Creative Commons License All site content, except where otherwise noted, is licensed under a Creative Commons Attribution 4.0 License.
PII: 4229