Open AccessSwainsonine Inhibits Invasion and the EMT Process in Esophageal Carcinoma Cells by Targeting Twist1
Author(s) -
Junxun Ma,
Lijie Wang,
Jinyu Li,
Guoqing Zhang,
Haitao Tao,
Xiaoyan Li,
Danyang Sun,
Yi Hu
Publication year - 2018
Publication title -
oncology research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.267
H-Index - 57
eISSN - 1555-3906
pISSN - 0965-0407
DOI - 10.3727/096504017x15046134836575
Subject(s) - swainsonine , apoptosis , cancer research , viability assay , biology , metastasis , esophageal cancer , pi3k/akt/mtor pathway , vimentin , cancer cell , gentamicin protection assay , cell , protein kinase b , cancer , medicine , immunology , biochemistry , immunohistochemistry
Esophageal cancer is a common gastrointestinal cancer, with a very high mortality rate in patients with metastasis. Swainsonine, a cytotoxic fungal alkaloid, has been shown to inhibit cell growth in esophageal cancer. In the present study, we explored the effects of swainsonine on cell invasion and metastasis in esophageal cancer cells. Human esophageal carcinoma cells were treated with different doses of swainsonine, and then cell viability, invasion, and apoptosis were measured. The mRNA and protein expressions of Twist1, apoptosis- and EMT-related factors, and PI3K/AKT pathway factors were detected by qRT-PCR and Western blot. Swainsonine had no effect on esophageal cancer cell viability and apoptosis, but it significantly decreased cell invasion in a dose-dependent manner. Swainsonine increased the expression of E-cadherin but decreased the expression of N-cadherin, vimentin, ZEB1, and snail in a dose-dependent manner, thereby inhibiting EMT. Last, we found that swainsonine inhibits cell invasion and EMT in the esophageal carcinoma cells by downregulation of Twist1 and deactivation of the PI3K/AKT signaling pathway.