Lei Deng1, Jun Zou2, Yongfeng Su1, Meijian Wang1, Lianwu Zhao3. 1. General Department of Oncology, Jiangxi Cancer Hospital, The Second Affiliated Hospital of Nanchang Medical College, Jiangxi Clinical Research Center for Cancer, Nanchang, 330029, Jiangxi, People's Republic of China. 2. Department of Abdominal Tumor Surgery, Jiangxi Cancer Hospital, The Second Affiliated Hospital of Nanchang Medical College, Jiangxi Clinical Research Center for Cancer, Nanchang, 330029, Jiangxi, People's Republic of China. 3. Department of Gastroenterology, Gaoxin Branch Of The First Affiliated Hospital Of Nanchang University, No. 7889 Changdong Ave, Gaoxin District, Nanchang, 330029, Jiangxi, People's Republic of China. zhaolianwu1986@163.com.
Abstract
OBJECTIVE: To investigate the effects of resveratrol (RSVL) on epithelial-mesenchymal transition (EMT) and biological behaviors of gastric cancer cells. METHODS: SGC-7901 cells were treated with RSVL, followed by TGF-β1 treatment for induction of EMT. Cell proliferation was tested by MTT assay, migration and invasion by Transwell and scratch assays, and Hippo-YAP signaling pathway activation by immunofluorescence. The RNA and protein expressions of E-cadherin, Vimentin, N-cadherin, and Snail were detected by qPCR and Western blot. A tumor model was constructed to examine the effect of RSVL on gastric tumor growth. RESULTS: RSVL inhibited the migration, invasion, and growth of gastric cancer cells in concentration- and time-dependent manners. RSVL inhibited TGF-β1-induced EMT of gastric cancer cells, which might relate to inactivation of the Hippo-YAP pathway. In the mouse tumor model, RSVL inhibited the EMT process by suppressing the Hippo-YAP pathway. CONCLUSION: RSVL inhibited EMT of gastric cancer cells probably by weakening the Hippo-YAP signaling pathway.
OBJECTIVE: To investigate the effects of resveratrol (RSVL) on epithelial-mesenchymal transition (EMT) and biological behaviors of gastric cancer cells. METHODS: SGC-7901 cells were treated with RSVL, followed by TGF-β1 treatment for induction of EMT. Cell proliferation was tested by MTT assay, migration and invasion by Transwell and scratch assays, and Hippo-YAP signaling pathway activation by immunofluorescence. The RNA and protein expressions of E-cadherin, Vimentin, N-cadherin, and Snail were detected by qPCR and Western blot. A tumor model was constructed to examine the effect of RSVL on gastric tumor growth. RESULTS: RSVL inhibited the migration, invasion, and growth of gastric cancer cells in concentration- and time-dependent manners. RSVL inhibited TGF-β1-induced EMT of gastric cancer cells, which might relate to inactivation of the Hippo-YAP pathway. In the mouse tumor model, RSVL inhibited the EMT process by suppressing the Hippo-YAP pathway. CONCLUSION: RSVL inhibited EMT of gastric cancer cells probably by weakening the Hippo-YAP signaling pathway.