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. 2019 Nov 5;11:9353–9369. doi: 10.2147/CMAR.S219689

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© 2019 Li et al.

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MST4 exerts the function through activating Ezrin signaling in GC. (A) STRING database showed the interaction of MST4 protein. (B) Protein expression of MST4, p-Ezrin and total Ezrin in GC cells with knockdown or overexpression of MST4. (C) Co-immunoprecipitation assays were performed to analyze the direct binding between MST4 and Ezrin in GC cells. (D) mRNA expression of Ezrin in GC cells with knockdown or overexpression of MST4. (E) Validate the expression of p-Ezrin in GC cell lines with overexpression of mutant T567D Ezrin or knockdown of Ezrin. (F) Transwell invasion assay was performed to determine Ezrin is a critical downstream effector in MST4-promoted invasion and metastasis in GC. (G) Immunofluorescence assays of cytoskeleton showed Ezrin is the key downstream effector of MST4-promoted F-actin filament rearrangement in GC cells. (H) Western blot tested the effect of Ezrin on EMT induced by MST4. (I) By knocking-in or -out of wild type Ezrin in corresponding GC cells, p-Ezrin and EMT markers were tested by Western blot. **P < 0.01; ***P < 0.001.