Oncotarget

Research Papers:

MiR-145 inhibits the epithelial-to-mesenchymal transition via targeting ADAM19 in human glioblastoma

Xingqiang Wang _, Enqin Wang, Jun Cao, Feng Xiong, Yonglin Yang and Haitao Liu

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Oncotarget. 2017; 8:92545-92554. https://doi.org/10.18632/oncotarget.21442

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Abstract

Xingqiang Wang1, Enqin Wang2, Jun Cao1, Feng Xiong1, Yonglin Yang1 and Haitao Liu1

1Department of Neurosurgery, Rizhao People’s Hospital, Jining Medical University, Rizhao 276826, Shandong, China

2Clinical Skill Training Center, Rizhao People’s Hospital, Jining Medical University, Rizhao 276826, Shandong, China

Correspondence to:

Xingqiang Wang, email: [email protected]

Keywords: MiR-145, ADAM19, GBM, EMT

Received: August 02, 2017     Accepted: August 28, 2017     Published: September 30, 2017

ABSTRACT

In recent years, increasing studies demonstrated that miR-145 plays a tumor suppressor role in many human cancers. In the present study, we evaluated the expression of miR-145 and A Disintegrin and Metalloproteinase 19 (ADAM19) in glioblastoma multiforme (GBM) tissues and cells. Furthermore, we investigated the mechanisms underlying miR-145/ADAM19-induced GBM biology. Here, we found that miR-145 expression was down-regulated, while ADAM19 expression was up-regulated in GBM tissues and cells. Moreover, miR-145 mimics repressed U87 and U251 cell proliferation, migration and invasion. miR-145 mimics also inhibited the epithelial-to-mesenchymal transition (EMT) of U87 and U251 cells. Mechanically, the 3’ untranslated region (3’-UTR) of ADAM19 mRNA was a direct target for miR-145. In addition, ADAM19 over-expression also partially abrogated miR-145-inhibited EMT. In conclusion, this work suggested that high miR-145 expression inhibited EMT of GBM cells by targeting ADAM19. Thus miR-145/ADAM19 can be suggested as a novel target for GBM patients.


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