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; Ming-Hsien Chien

doi:10.18632/oncotarget.4229

Oncotarget

Oncotarget (a primarily oncology-focused, peer-reviewed, open access journal) aims to maximize research impact through insightful peer-review; eliminate borders between specialties by linking different fields of oncology, cancer research and biomedical sciences; and foster application of basic and clinical science.

Its scope is unique. The term "oncotarget" encompasses all molecules, pathways, cellular functions, cell types, and even tissues that can be viewed as targets relevant to cancer as well as other diseases. The term was introduced in the inaugural Editorial, Introducing Oncotarget.

As of January 1, 2022, Oncotarget has shifted to a continuous publishing model. Papers will now be published continuously within yearly volumes in their final and complete form and then quickly released to Pubmed.

Subscribe to receive alerts once a paper has been published by Oncotarget.

Impact Journals, LLC is the publisher of Oncotarget: www.impactjournals.com.

Impact Journals is a member of the Wellcome Trust List of Compliant Publishers.

Impact Journals is a member of the Society for Scholarly Publishing.

On December 23, 2022, Oncotarget server experienced a DDoS attack. As a result, Oncotarget site was inaccessible for a few hours. Oncotarget team swiftly dealt with the situation and took it under control. This malicious action will be reported to the FBI.

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 2031 views | HTML 3135 views | ?

Abstract

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

Abstract

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.

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

Publication Alerts

Research Papers:

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

Abstract