Bufalin inhibits the growth and epithelial to mesenchymal transition of human gastric cancer cells via modulation of MEK/ERK pathway

Authors

  • Yi Zhou Department of General Surgery, Shidong Hospital, Yangpu District, Shanghai 200438, China.
  • Liguo Wang Department of General Surgery, Shidong Hospital, Yangpu District, Shanghai 200438, China.
  • Hui Lin Department of General Surgery, Shidong Hospital, Yangpu District, Shanghai 200438, China.
  • Yunxia Wang Department of General Surgery, Shidong Hospital, Yangpu District, Shanghai 200438, China.
  • Kezhu Hou Department of General Surgery, Shidong Hospital, Yangpu District, Shanghai 200438, China.

DOI:

https://doi.org/10.3329/bjp.v16i1.50548

Keywords:

Bufalin, Gastric cancer, MEK/ERK

Abstract

This study was designed to evaluate the anti-cancer effects of bufalin against the human gastric cancer cells and unveil the underlying mechanism. The results showed that bufalin inhibited the proliferation and colony formation of the MGC-803 gastric cancer cells and exhibited an IC50 of 10 μM. These antiproliferative effects were found to be due to the induction of G2/M cell cycle arrest. The G2/M cell cycle arrest was also concomitant with inhibition of cdc2, cdc25 and cyclin B1. Furthermore, bufalin suppressed the epithelial-to-mesenchymal transition, migration, and invasion of the MGC-803 gastric cancer cells. The Western blot analysis revealed that bufalin exerted its effects via deactivation of EK/ERK signaling pathway. Taken together, these results suggest the potential of bufalin as the lead molecule for the development of chemotherapy for gastric cancer.  

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Published

2021-01-05

How to Cite

Zhou, Y., L. Wang, H. Lin, Y. Wang, and K. Hou. “Bufalin Inhibits the Growth and Epithelial to Mesenchymal Transition of Human Gastric Cancer Cells via Modulation of MEK/ERK Pathway”. Bangladesh Journal of Pharmacology, vol. 16, no. 1, Jan. 2021, pp. 27-33, doi:10.3329/bjp.v16i1.50548.

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Research Articles