suppression of heregulin-β1her2-modulated invasive and aggressive phenotype of breast carcinoma by pterostilbene via inhibition of matrix metalloproteinase-9, p38 kinase cascade and akt activation英文论文.pdfVIP
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suppression of heregulin-β1her2-modulated invasive and aggressive phenotype of breast carcinoma by pterostilbene via inhibition of matrix metalloproteinase-9, p38 kinase cascade and akt activation英文论文
Hindawi Publishing Corporation
Evidence-Based Complementary and Alternative Medicine
Volume 2011, Article ID 562187, 12 pages
doi:10.1093/ecam/nep093
Original Article
Suppression of Heregulin-β 1/HER2-Modulated Invasive and
Aggressive Phenotype of Breast Carcinoma by Pterostilbene via
Inhibition of Matrix Metalloproteinase-9, p38 Kinase Cascade
and Akt Activation
Min-Hsiung Pan,1 Ying-Ting Lin,2 Chih-Li Lin,3 Chi-Shiang Wei,2 Chi-Tang Ho,4
and Wei-Jen Chen2
1 Department of Seafood Science, National Kaohsiung Marine University, Nan-Tzu, Kaohsiung, Taiwan
2 Department of Biomedical Sciences, Chung Shan Medical University, No. 110, Section 1, Chien-Kuo N. Road, Taichung 402, Taiwan
3 Institute of Medicine, Chung Shan Medical University, Taichung 402, Taiwan
4 Department of Food Science, Cook College, Rutgers University, New Brunswick, NJ, USA
Correspondence should be addressed to Wei-Jen Chen, cwj519@.tw
Received 26 April 2009; Accepted 25 June 2009
Copyright © 2011 Min-Hsiung Pan et al. This is an open access article distributed under the Creative Commons Attribution
License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly
cited.
Invasive breast cancer is the major cause of death among females and its incidence is closely linked to HER2 (human epidermal
growth factor receptor 2) overexpression. Pterostilbene, a natural analog of resveratrol, exerts its cancer chemopreventive
activity similar to resveratrol by inhibiting cancer cell proliferation and inducing apoptosis. However, the anti-invasive effect
of pterostilbene on HER2-bearing breast cancer has not been evaluated. Here, we used heregulin-β 1 (HRG-β 1), a ligand for
HER3, to transactivate HER2 signaling. We found that p
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