The inhibition effects of allicin on TGF-β1 induced epithelial⁃mesenchymal transition of human cholangiocarcinoma cell and its mechanism
10.16571/j.cnki.1008-8199.2019.02.006
- VernacularTitle: 大蒜素对TGF⁃β1诱导人胆管癌细胞上皮间质化的影响及机制
- Author:
Shi⁃qin ZHENG
1
;
Xiao⁃song WANG
1
;
Shuang CHEN
1
;
Zhan⁃peng YAN
2
;
Xiu⁃hua ZHANG
1
Author Information
1. Institute of Medical Center for Digestive Diseases, The Second Affiliated Hospital of Nanjing Medical University, Nanjing 210011,Jiangsu, China
2. Clinial Research Department of Chinese and Western Medicine, Jiangsu Province Hospital on Integration of Chinese and Western Medicine, Nanjing 210028, Jiangsu,China
- Publication Type:Journal Article
- Keywords:
cholangiocarcinoma;
allicin;
epithelial mesenchymal transition;
nuclear transcription factor
- From:
Journal of Medical Postgraduates
2019;32(2):143-147
- CountryChina
- Language:Chinese
-
Abstract:
Objective The metastasis mechanism of cholangiocarcinoma is complex, which may be related to epithelial-mesenchymal transition(EMT). This study focused on investigating the inhibition effects of allicin on TGF-β1 induced epithelium mesenchymal transition of human cholangiocarcinoma cells and its related mechanism, and providing theoretical basis for the application of allicin in the treatment of cholangiocarcinoma. Methods MTT assay were used to detect the inhibition effects of different concentrations of allicin on the human cholangiocarcinoma RBE cell proliferation, and the drug concentration of allicin was determined by IC50 of 24 h. The RBE cells were cultured and divided into control group, allicin group(130.7μmol/L), TGF-β1 group(10ng/mL) and allicin+ TGF-β1 group(130.7μmol/L+10ng/mL). Wound scratch and transwell invasion assay were performed to detect the migration and invasion ability of RBE cells after 24 hours. Western blots were applied to detect expression of EMT-related proteins (E-Cadherin, N-Cadherin, Vimentin, Snail) and NF-κB signaling pathways. Results The migration rates in allicin group and allicin+ TGF-β1 group were both decreased compared with that in the control group ( 9.25% ± 0.36% vs 28.19 %±0.66%, P<0.05) and TGF⁃β1 group(13.91%±0.75% vs 49.22%±0.27%, P<0.05). The invasion rates in allicin group and allicin+ TGF-β1 group were also decreased compared with that in the control group (6.59%±0.06% vs 33.48%±0.04%, P<0.05) and TGF⁃β1 group(9.4%± 0.05% vs 40.21%±0.12%, P<0.05). Compared with the control group, E-Cadherin expression was significantly increased, and N-Cadherin, Vimentin, Snail, NF-κB and p-NF-κB expression were significantly decreased in the allicin group (P<0.05). Compared with TGF-β1 group, E-Cadherin expression was significantly up-regulated, and N-Cadherin, Vimentin, Snail, NF-κB and p-NF-κB expression were significantly down-regulated in the allicin+ TGF-β1 group (P<0.05)． Conclusion These results indicate that allicin can inhibit the EMT induced by TGF-β1 on the human cholangiocarcinoma cell by blocking NF-κB signaling pathway, which may have potential value to be the drug candidate for the treatment of human cholangiocarcinoma in future.
