Abstract
Resveratrol (trans-3,4’,5-trihydroxystilbene), a natural polyphenolic compound detected in grapes, berries, and peanuts, possesses a wide spectrum of pharmacological properties, including anti-tumor metastasis activities. However, the underlying mechanisms through which resveratrol inhibits the metastasis of pancreatic cancer are still not fully elucidated. As epithelial-to-mesenchymal transition (EMT) is a key player for metastasis in tumor, the aim of this study is to determine whether resveratrol affects EMT in pancreatic cancer cells and the related mechanism. The results showed that resveratrol not only inhibited cell proliferation, migration, and invasion in a dose-dependent manner, but also mediated the expression of EMT-related genes (E-cadherin, N-cadherin, vimentin, MMP-2, and MMP-9) which are important for cancer cellular motility, invasiveness and metastasis during tumorigenesis. In addition, the levels of phospho-Akt and phospho- NF-κB in BxPC-3 and Panc-1 cells were reduced by both resveratrol and LY294002 (a PI3-K inhibitor). Furthermore, transforming growth factor-β (TGF-β)-induced alterations in cell morphology that are characteristic of EMT as well as increased cell invasive ability could also be reversed by resveratrol. Taken together, these data indicate that resveratrol suppresses pancreatic cancer migration and invasion through the inhibition of the PI-3K/Akt/NF-κB signaling pathway. This study suggests that resveratrol may be a potential anticancer agent for pancreatic cancer.
Keywords: Resveratrol, pancreatic cancer, invasion, metastasis, EMT, E-cadherin, PI-3K/Akt pathway, NF-κB pathway, TGF-β.
Current Medicinal Chemistry
Title:Resveratrol Inhibits the Epithelial-Mesenchymal Transition of Pancreatic Cancer Cells Via Suppression of the PI-3K/Akt/NF-κB Pathway
Volume: 20 Issue: 33
Author(s): Wei Li, Jiguang Ma, Qingyong Ma, Bin Li, Liang Han, Jiangbo Liu, Qinhong Xu, Wanxing Duan, Shuo Yu, Fengfei Wang and Erxi Wu
Affiliation:
Keywords: Resveratrol, pancreatic cancer, invasion, metastasis, EMT, E-cadherin, PI-3K/Akt pathway, NF-κB pathway, TGF-β.
Abstract: Resveratrol (trans-3,4’,5-trihydroxystilbene), a natural polyphenolic compound detected in grapes, berries, and peanuts, possesses a wide spectrum of pharmacological properties, including anti-tumor metastasis activities. However, the underlying mechanisms through which resveratrol inhibits the metastasis of pancreatic cancer are still not fully elucidated. As epithelial-to-mesenchymal transition (EMT) is a key player for metastasis in tumor, the aim of this study is to determine whether resveratrol affects EMT in pancreatic cancer cells and the related mechanism. The results showed that resveratrol not only inhibited cell proliferation, migration, and invasion in a dose-dependent manner, but also mediated the expression of EMT-related genes (E-cadherin, N-cadherin, vimentin, MMP-2, and MMP-9) which are important for cancer cellular motility, invasiveness and metastasis during tumorigenesis. In addition, the levels of phospho-Akt and phospho- NF-κB in BxPC-3 and Panc-1 cells were reduced by both resveratrol and LY294002 (a PI3-K inhibitor). Furthermore, transforming growth factor-β (TGF-β)-induced alterations in cell morphology that are characteristic of EMT as well as increased cell invasive ability could also be reversed by resveratrol. Taken together, these data indicate that resveratrol suppresses pancreatic cancer migration and invasion through the inhibition of the PI-3K/Akt/NF-κB signaling pathway. This study suggests that resveratrol may be a potential anticancer agent for pancreatic cancer.
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Cite this article as:
Li Wei, Ma Jiguang, Ma Qingyong, Li Bin, Han Liang, Liu Jiangbo, Xu Qinhong, Duan Wanxing, Yu Shuo, Wang Fengfei and Wu Erxi, Resveratrol Inhibits the Epithelial-Mesenchymal Transition of Pancreatic Cancer Cells Via Suppression of the PI-3K/Akt/NF-κB Pathway, Current Medicinal Chemistry 2013; 20 (33) . https://dx.doi.org/10.2174/09298673113209990251
DOI https://dx.doi.org/10.2174/09298673113209990251 |
Print ISSN 0929-8673 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-533X |
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