Publication: Metformin inhibits migration and invasion of cholangiocarcinoma cells
Issued Date
2017-02-01
Resource Type
ISSN
2476762X
15137368
15137368
Other identifier(s)
2-s2.0-85016465726
Rights
Mahidol University
Rights Holder(s)
SCOPUS
Bibliographic Citation
Asian Pacific Journal of Cancer Prevention. Vol.18, No.2 (2017), 473-477
Suggested Citation
Trinh Xuan Son, Nguyen Thi Bich Huyen, Kween Saimuang, Virapong Prachayasittikul, Waraporn Chan On Metformin inhibits migration and invasion of cholangiocarcinoma cells. Asian Pacific Journal of Cancer Prevention. Vol.18, No.2 (2017), 473-477. doi:10.22034/APJCP.2017.18.2.473 Retrieved from: https://repository.li.mahidol.ac.th/handle/20.500.14594/41982
Research Projects
Organizational Units
Authors
Journal Issue
Thesis
Title
Metformin inhibits migration and invasion of cholangiocarcinoma cells
Other Contributor(s)
Abstract
Background: Metformin is an oral anti-diabetic agent that has been widely prescribed for treatment of type II diabetes. Anti-cancer properties of metformin have been revealed for numerous human malignancies including cholangiocarcinoma (CCA) with anti-proliferative effects in vitro. However, effects on CCA cell migration and invasion have not been fully investigated. The present study aimed to explore the inhibitory effects of metformin on motility, migration and invasion of the CCA cell line HuCCT1, and examine molecular mechanisms underlying metformin effects. Methods: HuCCT1 cells were exposed to increasing doses of metformin. Viability and growth of HuCCT1 cells were assessed by MTS and colony formation assays, respectively. Motility, migration and invasion of metformin-treated HuCCT1 cells were determined in vitro using wound healing, transwell migration and matrigel invasion assays. Expression of signaling molecules and epithelial-mesenchymal transition (EMT) markers was assessed by Western blotting. Results: It was observed that metformin significantly decreased HuCCT1 cell viability and colony formation. The agent also markedly reduced wound closure, migration and invasion of HuCCT1 cells. Furthermore, metformin exposure resulted in decreased STAT3 activation and down-regulation of anti-apoptotic protein Bcl-2 and Mcl-1 expression. In addition, it upregulated the expression of E-cadherin, while downregulating that of N-cadherin, Snail, and MMP-2. Conclusion: These results demonstrated inhibitory effects of metformin on CCA cell migration and invasion, possibly involving the STAT3 pathway and reversal of EMT markers expression. They further suggest that metformin may be useful for CCA management.