Anillin Mediates EMT by Targeting c-Myc in the Nucleus and Potentiates Gastric Carcinoma Progression
FU Mingshi1, SHI Ke1, LIU Dongyang2, CHEN Feng2*
ANLN (Anillin), an actin-binding protein, reportedly plays a vital role in cell proliferation and migration, particularly in cytokinesis. Although there have been findings pointing to a contribution of ANLN to the development of cancer, the potential regulatory roles and molecular mechanisms by which ANLN affects the development and progression of GC (gastric carcinoma) remain obscure. Herein, applying wound healing assay, Transwell migration and Matrigel Trans-well assays to detect the effect of ANLN expression on migration and invasion ability of GC cells in vitro. Then, performing Western blot to evaluate EMT (epithelial-mesenchymal transition) associated proteins and Smad proteins. Moreover, performing immunofluorescence assay, Co-IP (co-immunoprecipitation) assay and Western blot to explore molecular mechanisms by which ANLN is involved in GC metastasis. In this study, ANLN silencing attenuated GC cell migration and invasion. Mechanistically, ANLN could interact with c-Myc in the nucleus and subsequently phosphorylate c-Myc to induce the expression of Snail and Slug transcription factors, to promote EMT but does not activate Smad proteins. Collectively, the data reveal a potential molecular mechanism in which ANLN mediates Smads signaling pathway and c-Myc protein respectively, which target downstream transcription factors (Snail and Slug) to trigger EMT.
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