Antitumor Effects of Rapamycin in Pancreatic Cancer Cells by Inducing Apoptosis and Autophagy

International Journal of Molecular Sciences

Zhi-Jun Dai¹  Jie Gao³  Xiao-Bin Ma²  Hua-Feng Kang²  Bao-Feng Wang²  Wang-Feng Lu²  Shuai Lin²  Xi-Jing Wang² 

[1] Department of Oncology, the Second Affiliated Hospital, Medical School of Xi’an Jiaotong University, Xi’an 710004, China; E-Mails:;Department of Nephrology, the Second Affiliated Hospital, Medical School of Xi’an Jiaotong University, Xi’an 710004, China; E-Mail:

关键词: pancreatic carcinoma;    rapamycin;    mTOR;    anti-tumor;    apoptosis;    autophagy;   

DOI  :  10.3390/ijms14010273

来源: mdpi

【 摘 要 】

Rapamycin (Rapa), an inhibitor of mammalian target of Rapamycin (mTOR), is an immunosuppressive agent that has anti-proliferative effects on some tumors. This study aims to investigate the effects of Rapa suppressing proliferation of pancreatic carcinoma PC-2 cells in vitro and its molecular mechanism involved in antitumor activities. MTT assays showed that the inhibition of proliferation of PC-2 cells in vitro was in a time- and dose-dependent manner. By using transmission electron microscopy, apoptosis bodies and formation of abundant autophagic vacuoles were observed in PC-2 cells after Rapa treatment. Flow cytometry assays also showed Rapa had a positive effect on apoptosis. MDC staining showed that the fluorescent density was higher and the number of MDC-labeled particles in PC-2 cells was greater in the Rapa treatment group than in the control group. RT-PCR revealed that the expression levels of p53, Bax and Beclin 1 were up-regulated in a dose-dependent manner, indicating that Beclin 1 was involved in Rapa induced autophagy and Rapa induced apoptosis as well as p53 up-regulation in PC-2 cells. The results demonstrated that Rapa could effectively inhibit proliferation and induce apoptosis and autophagy in PC-2 cells.

【 授权许可】

CC BY   
© 2013 by the authors; licensee Molecular Diversity Preservation International, Basel, Switzerland.