Research Papers:

This article has been corrected. Correction in: Oncotarget. 2017; 8:34018.

miR-424-5p promotes proliferation of gastric cancer by targeting Smad3 through TGF-β signaling pathway

Song Wei, Qing Li, Zheng Li, Linjun Wang, Lei Zhang and Zekuan Xu _

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Oncotarget. 2016; 7:75185-75196. https://doi.org/10.18632/oncotarget.12092

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Song Wei1,*, Qing Li1,*, Zheng Li1,*, Linjun Wang1, Lei Zhang1, Zekuan Xu1

1Department of General Surgery, The First Affiliated Hospital of Nanjing Medical University, Nanjing, Jiangsu, China

*These authors have contributed equally to this work

Correspondence to:

Zekuan Xu, email: [email protected]

Keywords: miR-424-5p, Smad3, proliferation, gastric cancer, TGF-β signaling pathway

Received: July 25, 2016    Accepted: September 10, 2016    Published: September 17, 2016


MiRNAs have been reported to regulate gene expression and be associated with cancer progression. Recently, miR-424-5p was reported to play important role in a variety of tumors. However, the role and molecular mechanisms of miR-424-5p in GC (gastric cancer) remains largely unknown. In this study, we aimed to explore the role of miR-424-5p in GC. QRT-PCR was used to determine the expression levels of miR-424-5p and Smad3. CCK8 assay, plate clone assay and cell cycle assay were used to measure the effects of miR-424-5p on GC cell proliferation. Luciferase reporter assay and western blotting were used to prove that Smad3 was one of the direct targets of miR-424-5p. Tumorigenesis assay was used to investigate the role of miR-424-5p in tumor growth of GC cells in vivo. We found that miR-424-5p was up-regulated in GC tissues and cells. Over-expression of miR-424-5p could promote the proliferation of GC cells. In addition, luciferase reporter assay and western blotting assay revealed that Smad3 was a direct target of miR-424-5p. Over-expression of Smad3 could partially reverse the effects of miR-424-5p on GC cell proliferation. Our study further revealed that miR-424-5p could inhibit TGF-β signaling pathway by Smad3.

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