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28.09.2016 | Original Article | Ausgabe 11/2016

Tumor Biology 11/2016

Direct targeting of HGF by miR-16 regulates proliferation and migration in gastric cancer

Tumor Biology > Ausgabe 11/2016
Shuang Li, Haiyang Zhang, Xinyi Wang, Yanjun Qu, Jingjing Duan, Rui Liu, Ting Deng, Tao Ning, Le Zhang, Ming Bai, Likun Zhou, Xia Wang, Shaohua Ge, Guoguang Ying, Yi Ba
Wichtige Hinweise

Electronic supplementary material

The online version of this article (doi:10.​1007/​s13277-016-5390-6) contains supplementary material, which is available to authorized users.
Shuang Li, Haiyang Zhang, Xinyi Wang, Yanjun Qu, and Jingjing Duan contribute to this work equally.


MicroRNAs (miRNAs) have been reported to be involved in each stage of tumor development in various types of cancers. We have previously showed that miR-16 is downregulated in cancer and acts as a tumor suppressor. Other studies indicated that hepatocyte growth factor (HGF)/c-Met is implicated in proliferation, migration, and other pathophysiological processes. However, little is known about the relationship between miR-16 and HGF/c-Met in gastric cancer (GC). In the present study, we used bioinformatics tools and related experiments to search for miRNAs targeting HGF. Here, we found that miR-16 suppressed HGF protein expression by directly targeting 3′-untranslated region (UTR) of HGF mRNA. Subsequently, it was illustrated the downregulation of miR-16 promotes, while overexpressed of miR-16 significantly inhibits cell proliferation and migration by negatively regulating HGF/c-Met pathway. Moreover, the biological role of HGF in GC cells was determined by using HGF siRNA and HGF-overexpressing plasmid, respectively. To conclude, our results provide a potential target by using miR-16 for the future clinical treatment of GC.

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