Marsdenia tenacissima extract suppresses A549 cell migration through regulation of CCR5-CCL5 axis, Rho C, and phosphorylated FAK.
10.1016/S1875-5364(16)30017-6
- Author:
Sen-Sen LIN
1
;
Fang-Fang LI
1
;
Li SUN
2
;
Wei FAN
1
;
Ming GU
1
;
Lu-Yong ZHANG
1
;
Song QIN
3
;
Sheng-Tao YUAN
4
Author Information
1. New Drug Screen Center, China Pharmaceutical University, Nanjing 210009, China.
2. New Drug Screen Center, China Pharmaceutical University, Nanjing 210009, China. Electronic address: cpusunli@126.com.
3. Nanjing Sanhome Pharmaceutical Co., Ltd., Nanjing, 210046, China.
4. New Drug Screen Center, China Pharmaceutical University, Nanjing 210009, China. Electronic address: yuanst@aliyun.com.
- Publication Type:Journal Article
- Keywords:
A549 cell migration;
CCR5-CCL5 axis;
FAK;
Rho C;
XAP
- MeSH:
A549 Cells;
Antineoplastic Agents, Phytogenic;
pharmacology;
Cell Line, Tumor;
Cell Movement;
drug effects;
Chemokine CCL5;
metabolism;
Focal Adhesion Kinase 1;
metabolism;
Humans;
Lung Neoplasms;
Marsdenia;
chemistry;
Phosphorylation;
Plant Extracts;
pharmacology;
Receptors, CCR5;
metabolism;
rho GTP-Binding Proteins;
metabolism;
rhoC GTP-Binding Protein
- From:
Chinese Journal of Natural Medicines (English Ed.)
2016;14(3):203-209
- CountryChina
- Language:English
-
Abstract:
Marsdenia tenacissima, a traditional Chinese medicine, is long been used to treat various diseases including asthma, cancer, trachitis, tonsillitis, pharyngitis, cystitis, and pneumonia. Although Marsdenia tenacissima has been demonstrated to have strong anti-tumor effects against primary tumors, its effect on cancer metastasis remains to be defined, and the molecular mechanism underlying the anti-metastatic effect is unknown. In the present study, we investigated the effects of XAP (an extract of Marsdenia tenacissima) on A549 lung cancer cell migration and explored the role of CCR5-CCL5 axis in the anti-metastatic effects of XAP. Our resutls showed that XAP inhibited A549 lung cancer cell migration and invasion in a dose-dependent manner. The protein levels of CCR5, but not CCR9 and CXCR4, were decreased by XAP. The secretion of CCL5, the ligand of CCR5, was reduced by XAP. XAP down-regulated Rho C expression and FAK phosphorylation. In conclusion, XAP inhibited A549 cell migration and invasion through down-regulation of CCR5-CCL5 axis, Rho C, and FAK.
