Research Papers:

Salen-Mn compounds induces cell apoptosis in human prostate cancer cells through promoting AMPK activity and cell autophagy

Xiaoshuang Tang, Jing Jia, Feng Li, Wei Liu, Chao Yang, Bin Jin, Qi Shi, Xinyang Wang, Dalin He and Peng Guo _

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Oncotarget. 2017; 8:86277-86286. https://doi.org/10.18632/oncotarget.21138

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Xiaoshuang Tang1,2,*, Jing Jia1,*, Feng Li1, Wei Liu1, Chao Yang1, Bin Jin1, Qi Shi1, Xinyang Wang1,3,4, Dalin He1,3,4 and Peng Guo1,3,4

1Department of Urology, The First Affiliated Hospital of Xi’an Jiaotong University, Xi’an, Shaanxi, China

2Department of Urology, The Second Affiliated Hospital of Xi’an Jiaotong University, Xi’an, Shaanxi, China

3Key Laboratory for Tumor Precision Medicine of Shaanxi Province, Xi’an, Shaanxi, China

4Oncology Research Lab, Key Laboratory of Environment and Genes Related to Diseases, Ministry of Education, Xi’an, Shaanxi, China

*These authors have contributed equally to this work

Correspondence to:

Peng Guo, email: [email protected]

Dalin He, email: [email protected]

Keywords: salen-Mn, prostate cancer, cell apoptosis, AMPK, autophagy

Received: January 23, 2017     Accepted: August 26, 2017     Published: September 21, 2017


Currently only docetaxel has been approved to be used in the chemotherapy of prostate cancer and new drugs are urgent need. Salen-Mn is a novel type of synthetic reagent bionic and exerts remarkable anticancer activities. However, the effect of Salen-Mn on human prostate cancer has not been elucidated yet. In this study, we found that treatment of PC-3 and DU145 human prostate cancer cells with Salen-Mn inhibited cell growth in dose and time dependent manner. Moreover, Salen-Mn induced cell apoptosis, and increased the expression of apoptotic proteins, such as cleaved caspase-3, cleaved PARP, and Bax, in PC-3 and DU145 prostate cancer cells. Furthermore, we found that Salen-Mn induced expression of LC3-I/II, which is protein marker of cell autophagy, in both dose and time dependent manners; in addition, Salen-Mn increased the phosphorylation of AMPK, suggesting that Salen-Mn increase cell autophagy through activating AMPK pathway. On the other hand, when PC-3 and DU145 cells were treated with Salen-Mn and 3-MA, an inhibitor of cell autophagy, the inhibitory effect of Salen-Mn on cell growth and the induction of apoptotic proteins were decreased. In addition, we found that Salen-Mn inhibited the growth of PC-3 cell xenografts in nude mice. In summary, our results indicate that Salen-Mn suppresses cell growth through inducing AMPK activity and autophagic cell death related cell apoptosis in prostate cancer cells and suggest that Salen-Mn and its derivatives could be new options for the chemical therapeutics in the treatment of prostate cancer.

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