p53 Is a Key Regulator for Osthole-Triggered Cancer PathogenesisReport as inadecuate




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BioMed Research InternationalVolume 2014 2014, Article ID 175247, 9 pages

Research Article

Graduate Institute of Biotechnology, National Chung Hsing University, Taichung 402, Taiwan

Preventive Medicine Center, Department of Community Medicine, Taichung Tzu Chi Hospital, Buddhist Tzu Chi Medical Foundation, Taichung 427, Taiwan

Division of Colon and Rectal Surgery, Department of Surgery, Taichung Tzu Chi Hospital, Buddhist Tzu Chi Medical Foundation, Taichung 427, Taiwan

School of Medicine, Tzu Chi University, Hualien 970, Taiwan

Department of Biotechnology, Asia University, Taichung 413, Taiwan

Comprehensive Breast Cancer Center, Changhua Christian Hospital, Changhua 500, Taiwan

Department of Cell and Tissue Engineering, Changhua Christian Hospital, Changhua 500, Taiwan

Received 11 May 2014; Revised 22 May 2014; Accepted 22 May 2014; Published 12 June 2014

Academic Editor: Shun-Fa Yang

Copyright © 2014 Ssu-Ming Huang et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Osthole has been reported to have antitumor activities via the induction of apoptosis and inhibition of cancer cell growth and metastasis. However, the detailed molecular mechanisms underlying the anticancer effects of osthole in human colon cancer remain unclear. In the present study, we have assessed osthole-induced cell death in two different human colon cancer cell lines, HCT116 and SW480. Our results also showed that osthole activated proapoptotic signaling pathways in human colon cancer cells. By using cell culture insert system, osthole reduced cell motility in both human colon cancer cell lines. This study also provides evidence supporting the potential of osthole in p53 activation. Expression of p53, an apoptotic protein, was remarkably upregulated in cells treated with osthole. Importantly, the levels of phosphorylation of p53 on Ser15 p-p53 and acetylation of p53 on Lys

acetyl-p53 were increased under osthole treatment. Our results also demonstrated that p53 was activated followed by generation of reactive oxygen species ROS and activation of c-Jun N-terminal kinase JNK. Our study provides novel insights of p53-mediated responses under osthole treatment. Taken together, we concluded that osthole induces cancer cell death and inhibits migratory activity in a controlled manner and is a promising candidate for antitumor drug development.





Author: Ssu-Ming Huang, Cheng-Fang Tsai, Dar-Ren Chen, Min-Ying Wang, and Wei-Lan Yeh

Source: https://www.hindawi.com/



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