15,16-Dihydrotanshinone I, a Compound of Salvia miltiorrhiza Bunge, Induces Apoptosis through Inducing Endoplasmic Reticular Stress in Human Prostate Carcinoma CellsReportar como inadecuado




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Evidence-Based Complementary and Alternative MedicineVolume 2011 2011, Article ID 865435, 9 pages

Research Article

Department of Surgery, St. Martin De Porres Hospital, Chia-Yi City 60069, Taiwan

Department of Internal Medicine, Taoyuan General Hospital, Taoyuan 33004, Taiwan

Department of Biomedical Engineering, Chung Yuan Christian University, Chung-Li 32023, Taiwan

Department of Urology, Taipei Medical University Hospital, Taipei 11031, Taiwan

School of Medical Laboratory Science and Biotechnology, College of Medical Science and Technology, Taipei Medical University, Taipei 11031, Taiwan

Department of Primary Care Medicine, Taipei Medical University Hospital, Taipei 11031, Taiwan

Division of Gastroenterology, Department of Internal Medicine, Wan Fang Hospital, Taipei Medical University, Taipei 11696, Taiwan

Traditional Herbal Medicine Research Center, Taipei Medical University Hospital, Taipei 11031, Taiwan

Received 8 September 2010; Accepted 21 December 2010

Copyright © 2011 Mao-Te Chuang 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

5,16-dihydrotanshinone I DHTS is extracted from Salvia miltiorrhiza Bunge tanshen root and was found to be the most effective compound of tanshen extracts against breast cancer cells in our previous studies. However, whether DHTS can induce apoptosis through an endoplasmic reticular ER stress pathway was examined herein. In this study, we found that DHTS significantly inhibited the proliferation of human prostate DU145 carcinoma cells and induced apoptosis. DHTS was able to induce ER stress as evidenced by the upregulation of glucose regulation protein 78 GRP78-Bip and CAAT-enhancer binding protein homologous protein-growth arrest- and DNA damage-inducible gene 153 CHOP-GADD153, as well as increases in phosphorylated eukaryotic initiation factor 2α eIF2α, c-jun N-terminal kinase JNK, and X-box-binding protein 1 XBP1 mRNA splicing forms. DHTS treatment also caused significant accumulation of polyubiquitinated proteins and hypoxia-inducible factor HIF-1α, indicating that DHTS might be a proteasome inhibitor that is known to induce ER stress or enhance apoptosis caused by the classic ER stress-dependent mechanism. Moreover, DHTS-induced apoptosis was reversed by salubrinal, an ER stress inhibitor. Results suggest that DHTS can induce apoptosis of prostate carcinoma cells via induction of ER stress and-or inhibition of proteasome activity, and may have therapeutic potential for prostate cancer patients.





Autor: Mao-Te Chuang, Feng-Ming Ho, Chien-Chih Wu, Shao-Yu Zhuang, Shyr-Yi Lin, Fat-Moon Suk, and Yu-Chih Liang

Fuente: https://www.hindawi.com/



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