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BioMed Research International
Volume 2017 (2017), Article ID 7203584, 6 pages
Research Article

Zoledronic Acid Regulates Autophagy and Induces Apoptosis in Colon Cancer Cell Line CT26

1Jiangsu Health Vocational College, Nanjing, Jiangsu, China
2College of Medicine, Nanjing University, Nanjing, Jiangsu, China
3School of Pharmacy, Nanjing University of Chinese Medicine, Nanjing, Jiangsu, China

Correspondence should be addressed to Wei Zhang

Received 1 July 2017; Revised 2 November 2017; Accepted 10 December 2017; Published 31 December 2017

Academic Editor: Luciana Dini

Copyright © 2017 Jinhua Zhu 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.


Zoledronic acid (ZOL) is the third generation of bisphosphonates, which can inhibit many tumors growth, especially to inhibit the growth of colon cancer. However, the molecular mechanism is still very mysterious. In this study, we observed that ZOL could regulate CT26 colon cancer cells autophagy, promote CT26 cells apoptosis, and inhibit CT26 cells proliferation. Western blotting analysis showed that proapoptosis protein caspase-3 was basically unchanged, whereas the expression of the activated caspase-3 was significantly increased, after CT26 cells were treated with different doses of zoledronic acid. Western blot also showed that ZOL could significantly affect the expression of p-p53 and autophagy-related proteins beclin-1 and p62. In conclusion, the antitumor effect of ZOL on CT26 colon cancer cells in vitro is achieved by apoptosis induction and autophagy regulation, resulting in inhibition of cell proliferation.