Ginsenoside Rg1 attenuates invasion and migration by inhibiting transforming growth factor-β1-induced epithelial to mesenchymal transition in HepG2 cells

被引:47
作者
Yu, Meiling [1 ,2 ]
Yu, Xiaobing [3 ]
Guo, Daohua [1 ,2 ]
Yu, Binbin [2 ]
Li, Li [3 ]
Liao, Qiao [2 ]
Xing, Rong [1 ,2 ]
机构
[1] Bengbu Med Coll, Affiliated Hosp 1, Dept Pharm, Bengbu 233004, Anhui, Peoples R China
[2] Bengbu Med Coll, Fac Pharm, Bengbu 233030, Anhui, Peoples R China
[3] Sun Yat Sen Univ, Zhongshan Sch Med, Dept Pharmacol, Guangzhou 510080, Guangdong, Peoples R China
基金
中国博士后科学基金;
关键词
transforming growth factor-1; epithelial to mesenchymal transition; ginsenoside Rg1; invasion; migration; TRANSDIFFERENTIATION; PROTECTS; MODEL; BETA;
D O I
10.3892/mmr.2014.3098
中图分类号
R73 [肿瘤学];
学科分类号
100214 [肿瘤学];
摘要
Ginseng has become one of the most commonly used alternative herbal medicines and its active component, ginsenoside Rg1, possesses known pharmacological effects, including anticancer properties. However, the effects of ginsenoside Rg1 on metastasis have not been investigated. The present study demonstrated that ginsenoside Rg1 was able to suppress transforming growth factor-1 (TGF-1)-induced invasion and migration in HepG2 liver cancer cells. This suppression was associated with the inhibition of TGF-1-induced epithelial to mesenchymal transition (EMT). Furthermore, TGF-1 induced HepG2 cells to undergo EMT and significantly promoted cell invasion and migration. When cells were pretreated with ginsenoside Rg1 for 24 h and subsequently exposed to TGF-1 for 24 h, the results demonstrated that ginsenoside Rg1 inhibited the initiation of TGF-1-induced EMT. In addition, HepG2 cells exhibited a mesenchymal phenotype when exposed to TGF-1, but when exposed to ginsenoside Rg1 this effect was reversed and the cells exhibited a classical epithelial morphology. Ginsenoside Rg1 also increased the expression of the epithelial phenotype marker E-cadherin and repressed the expression of the mesenchymal phenotype marker vimentin. In conclusion, the results of the present study suggest that ginsenoside Rg1 may suppress liver cancer invasion and migration in vitro through inhibiting TGF-1-induced EMT.
引用
收藏
页码:3167 / 3173
页数:7
相关论文
共 27 条
[1]
Ginseng pharmacology - Multiple constituents and multiple actions [J].
Attele, AS ;
Wu, JA ;
Yuan, CS .
BIOCHEMICAL PHARMACOLOGY, 1999, 58 (11) :1685-1693
[2]
A Perspective on Cancer Cell Metastasis [J].
Chaffer, Christine L. ;
Weinberg, Robert A. .
SCIENCE, 2011, 331 (6024) :1559-1564
[3]
p53 regulates epithelial-mesenchymal transition and stem cell properties through modulating miRNAs [J].
Chang, Chun-Ju ;
Chao, Chi-Hong ;
Xia, Weiya ;
Yang, Jer-Yen ;
Xiong, Yan ;
Li, Chia-Wei ;
Yu, Wen-Hsuan ;
Rehman, Sumaiyah K. ;
Hsu, Jennifer L. ;
Lee, Heng-Huan ;
Liu, Mo ;
Chen, Chun-Te ;
Yu, Dihua ;
Hung, Mien-Chie .
NATURE CELL BIOLOGY, 2011, 13 (03) :317-U296
[4]
CEACAM6 induces epithelial-mesenchymal transition and mediates invasion and metastasis in pancreatic cancer [J].
Chen, Jianmin ;
Li, Qiang ;
An, Yong ;
Lv, Nan ;
Xue, Xiaofeng ;
Wei, Jishu ;
Jiang, Kuirong ;
Wu, Junli ;
Gao, Wentao ;
Qian, Zhuyin ;
Dai, Cuncai ;
Xu, Zekuan ;
Miao, Yi .
INTERNATIONAL JOURNAL OF ONCOLOGY, 2013, 43 (03) :877-885
[5]
Creighton Chad J, 2013, Cancer Manag Res, V5, P187, DOI 10.2147/CMAR.S35171
[6]
Ellenrieder V, 2001, CANCER RES, V61, P4222
[7]
Hallmarks of Cancer: The Next Generation [J].
Hanahan, Douglas ;
Weinberg, Robert A. .
CELL, 2011, 144 (05) :646-674
[8]
Cancer statistics, 2005 [J].
Jemal, A ;
Murray, T ;
Ward, E ;
Samuels, A ;
Tiwari, RC ;
Ghafoor, A ;
Feuer, EJ ;
Thun, MJ .
CA-A CANCER JOURNAL FOR CLINICIANS, 2005, 55 (01) :10-30
[9]
Ginsenoside rg1 enhances CD4+ T-cell activities and modulates Th1/Th2 differentiation [J].
Lee, EJ ;
Ko, EJ ;
Lee, JW ;
Rho, SW ;
Ko, SG ;
Shin, MK ;
Min, BI ;
Hong, MC ;
Kim, SY ;
Bae, HS .
INTERNATIONAL IMMUNOPHARMACOLOGY, 2004, 4 (02) :235-244
[10]
The epithelial-mesenchymal transition: new insights in signaling, development, and disease [J].
Lee, JM ;
Dedhar, S ;
Kalluri, R ;
Thompson, EW .
JOURNAL OF CELL BIOLOGY, 2006, 172 (07) :973-981