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      TRPC1/3/6 inhibition attenuates the TGF-β1-induced epithelial-mesenchymal transition in gastric cancer via the Ras/Raf1/ERK signaling pathway : TRPC1/3/6 in TGF-β1-induced EMT in SGC-7901 cells

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          Most cited references15

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          Epithelial-mesenchymal transitions in development and disease.

          The epithelial to mesenchymal transition (EMT) plays crucial roles in the formation of the body plan and in the differentiation of multiple tissues and organs. EMT also contributes to tissue repair, but it can adversely cause organ fibrosis and promote carcinoma progression through a variety of mechanisms. EMT endows cells with migratory and invasive properties, induces stem cell properties, prevents apoptosis and senescence, and contributes to immunosuppression. Thus, the mesenchymal state is associated with the capacity of cells to migrate to distant organs and maintain stemness, allowing their subsequent differentiation into multiple cell types during development and the initiation of metastasis.
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            Mechanisms of TGF-β Signaling from Cell Membrane to the Nucleus

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              International Union of Pharmacology. XLIX. Nomenclature and structure-function relationships of transient receptor potential channels.

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                Author and article information

                Journal
                Cell Biology International
                Cell Biol Int
                Wiley
                10656995
                August 2018
                August 2018
                May 10 2018
                : 42
                : 8
                : 975-984
                Affiliations
                [1 ]Department of Gastrointestinal Surgery; The Affiliated Hospital of Binzhou Medical University; No. 666 Yellow River Road Binzhou 256603 China
                [2 ]Department of Nephrology; Second Affiliated Hospital of Xi'an Jiaotong University; Xi'an 710004 China
                Article
                10.1002/cbin.10963
                29570903
                f4f2d8cc-4f3b-4f18-af07-0595d2393b90
                © 2018

                http://doi.wiley.com/10.1002/tdm_license_1.1

                http://onlinelibrary.wiley.com/termsAndConditions#vor

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