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Abstract
Background: To understand the function of β6 integrin and elucidate its signaling pathways in TGF-β-induced EMT in breast cancer. Methods: The interactions between TGF-β1 and β6 integrin were measured by coimmunoprecipitation. The EMT responses, phospherlation of PI3K/Akt and COX-2 expression were determined by real-time PCR, transwell assay, and western blot after the blockage of β6 integrin. Results: TGF-β1 and β6 integrin could bind with each other. Blockage of β6 integrin rescued TGF-β1-induced EMT phenotype and reduced expression of COX-2 via dephosphorylation of PI3K/Akt. Conclusions: β6 integrin plays a critical role in TGF-β1-induced EMT and overexpression of COX-2 in breast cancer.
ACKNOWLEDGMENTS
This study was supported by grants from National Nature Scientific Foundation of China (81072068) and The Natural Science Foundation of Shandong Province (BS2011YY060). The funding sources had no involvement in study design; in the collection, analysis and interpretation of data or in the decision to submit the article for publication. Dr. Wentong Li wrote the manuscript and carried out the experiments; Dr. Baogang Zhang performed the interaction between integrin and TGF; Dr. Chunling Zhao and Hongli Li participated in construction of expression plasmids and cells culture; Dr. Yanmei Zhong performed Real-time PCR. Jing Sun participated in Western Blot assays and Dr. Shijun Lv participated in statistical analysis. All authors read and approved the final manuscript.