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.
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