Research Papers:

Traditional Chinese medicine Ka-Sai-Ping suppresses the growths of gastric cancers via induction of autophagy

Mo-Li Zhu, Jun-Xiu Lu, Guo-Pin Pan, Song Ping, Fan-Rong Zhao, Heng-Tian Qi, Hai-Ya Yu, Xu Jian, Guang-Rui Wan and Peng Li _

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Oncotarget. 2017; 8:95075-95082. https://doi.org/10.18632/oncotarget.18041

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Mo-Li Zhu1,*, Jun-Xiu Lu2,*, Guo-Pin Pan1, Song Ping1, Fan-Rong Zhao3, Heng-Tian Qi4, Hai-Ya Yu5, Xu Jian1, Guang-Rui Wan1 and Peng Li1

1College of Pharmacy, Xinxiang Medical University, Xinxiang, China

2Department of Histology and Embryology, Xinxiang Medical University, Xinxiang, China

3San-Quan College of Xinxiang Medical University, Xinxiang, China

4Department of Cardiothoracic Surgery, The Third Affiliated Hospital, Xinxiang Medical University, Xinxiang, China

5Department of Neurology, The People’s Hospital of Xishui County, Huangang, Hubei, China

*These authors contributed equally to this work

Correspondence to:

Peng Li, email: [email protected]

Keywords: traditional Chinese medicine, Ka-Sai-Ping, gastric cancer, autophagy, apoptosis

Received: March 17, 2017     Accepted: May 10, 2017     Published: May 20, 2017


Traditional Chinese medication is increasingly used to treat a wide range of human chronic diseases like cardiovascular diseases and cancers. This study was designed to explore whether ka-sai-ping (KSP), a novel traditional Chinese medicine developed by us, prevents gastric cancer growths and to investigate the underlying mechanism. The xenograft model of mouse gastric cancer was established by injecting MFCs into nude mouse subcutaneously. Cell autophagy was assessed by MDC staining. Lysosome and mitochondria were detected by Lyso-Tracker Red and Mito-Traker Green staining. Incubation of cultured mouse gastric cancer cell line MFCs with KSP for 48 hours, concentration-dependently reduced cell survivals and activated autophagy, which were accompanied with damaged lysosomes and mitochondria. In vivo studies indicated that KSP therapy (20 ml/kg/day) for two weeks suppressed the growth of gastric cancer, increased the protein levels of LC3-II, beclin-1, cathepsin L, bcl-2, p53, and capase-3 in tumor tissues from the xenograft model of mouse gastric cancer. Importantly, all these effects induced by KSP were abolished by co-administration of autophagy inhibitor 3-MA. In conclusion, KSP activates cell autophagy to suppress gastric cancer growths. Clinically, KSP is potentially considered as a medicine to treat patients with gastric cancer.

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