Research Papers:

The component formula of Salvia miltiorrhiza and Panax ginseng induces apoptosis and inhibits cell invasion and migration through targeting PTEN in lung cancer cells

Lei Bi, Xiaojing Yan, Ye Yang, Lei Qian, Yuan Tian, Jian-Hua Mao and Weiping Chen _

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Oncotarget. 2017; 8:101599-101613. https://doi.org/10.18632/oncotarget.21354

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Lei Bi1,2,4,*, Xiaojing Yan3,*, Ye Yang1, Lei Qian1, Yuan Tian1, Jian-Hua Mao2 and Weiping Chen1

1School of Preclinical Medicine, Nanjing University of Chinese Medicine, Nanjing 210023, China

2Biological Systems and Engineering Division, Lawrence Berkeley National Laboratory, Berkeley, CA 94720, USA

3Changzhou Affiliated Hospital, Nanjing University of Chinese Medicine, Changzhou 213003, China

4Jiangsu Collaborative Innovation Center of Traditional Chinese Medicine (TCM) Prevention and Treatment of Tumor, Nanjing University of Chinese Medicine, Nanjing 210023, China

*These authors have contributed equally to this work

Correspondence to:

Weiping Chen, email: [email protected]

Jian-Hua Mao, email: [email protected]

Keywords: the component formula of Salvia miltiorrhiza and Panax ginseng (FMG); orthogonal array design; PTEN phosphorylation; PI3K/AKT signaling pathway

Received: January 11, 2017    Accepted: August 28, 2017    Published: September 28, 2017


Lung cancer still remains the leading cause of cancer-related death worldwide. It is an urgent need for development of novel therapeutic agents to improve current treatment of this disease. Here we investigate whether the effective component formula of traditional Chinese Medicine could serve as new potential therapeutic drugs to treat lung cancer. We optimize the most effective component formula of Salvia miltiorrhiza and Panax Ginseng (FMG), which is composed of Salvianolic acid A, 20(S)-Ginsenoside and Ginseng polysaccharide. We discovered that FMG selectively inhibited lung cancer cell proliferation and induced apoptosis but had no any cytotoxic effects on normal lung epithelial BEAS-2B cells. Moreover, FMG inhibited lung cancer cell migration and invasion. Mechanistically, we found that FMG significantly promoted p-PTEN expression and subsequently inhibited PI3K/AKT signaling pathway. The phosphatase activity of PTEN protein was increased after FMG bound to PTEN protein, indicating that PTEN is one of the FMG targeted proteins. In addition, FMG regulated expression of some marker proteins relevant to cell apoptosis, migration and invasion. Collectively, these results provide mechanistic insight into the anti-NSCLC of FMG by enhancing the phosphatase activity of PTEN, and suggest that FMG could be as a potential option for lung cancer treatment.

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