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. 2019 Apr 23;11:3493–3509. doi: 10.2147/CMAR.S195137

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© 2019 Liu et al.

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SMARCE1 increases GC cell proliferation, migration, and invasion via activation of the MAPK/ERK signaling pathway.

Notes: (A) The protein expression of SMARCE1, ERK1/2, p-ERK1/2, MMP9, and cyclin D1 was examined through western blotting. β-actin was used as control. (B) The relative protein expression was analyzed using the gray level and presented as mean ± SD. (C) The CCK-8 assay detected the proliferation of MGC-803^SMARCE1, AGS^shSMARCE1, and control cells treated with 10 μM of U0126 – an inhibitor of the MAPK/ERK signaling pathway or DMSO. U0126 blocked the proliferation of GC cells induced by SMARCE1. (D) A wound healing assay was performed to evaluate the migration ability of MGC-803^SMARCE1, AGS^shSMARCE1, and control cells with or without U0126 treatment. U0126 abrogated the SMARCE1-induced GC cell migration. (E) The invasion ability of MGC-803^SMARCE1, AGS^shSMARCE1, and control cells was determined using a transwell invasion assay. Cell invasion triggered by SMARCE1 was almost completely abolished following treatment with U0126. (F) Quantification of wound closure was shown. (G) Quantification of invasion ability was shown. All data are shown as mean ± SD. Magnification ×100; *P<0.05; **P<0.01; ***P<0.001.

Abbreviations: p-ERK1/2, phosphorylated ERK1/2; MMP9, matrix metalloproteinase 9; DMSO, dimethyl sulfoxide; GC, gastric cancer.