Oncotarget

Research Papers:

miR-93 promotes cell proliferation in gliomas through activation of PI3K/Akt signaling pathway

Lili Jiang _, Chanjuan Wang, Fangyong Lei, Longjuan Zhang, Xin Zhang, Aibin Liu, Geyan Wu, Jinrong Zhu and Libing Song

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Oncotarget. 2015; 6:8286-8299. https://doi.org/10.18632/oncotarget.3221

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Abstract

Lili Jiang1,2, Chanjuan Wang3, Fangyong Lei2, Longjuan Zhang4, Xin Zhang2, Aibin Liu5, Geyan Wu5, Jinrong Zhu5, Libing Song2

1Department of Pathophysiology, Guangzhou Medical University, Guangzhou 510182, China

2State Key Laboratory of Oncology in Southern China, Department of Experimental Research, Cancer Centre, Sun Yat-sen University, Guangzhou 510060, China

3Department of the Central Laboratory, The First Affiliated Hospital/School of Clinical Medicine of Guangdong Pharmaceutical University, Guangzhou 510080, China

4Laboratory of Surgery, First Affiliated Hospital, Sun Yat-sen University, Guangzhou 510080, China

5Department of Biochemistry, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou, Guangdong 510080, China

Correspondence to:

Libing Song, e-mail: lb.song1@gmail.com

Lili Jiang, e-mail: jianglili126@163.com

Keywords: PI3K/Akt, miR-93, gliomas

Received: December 02, 2014     Accepted: January 26, 2015     Published: March 13, 2015

ABSTRACT

The PI3K/Akt signaling pathway is frequently activated in various human cancer types and plays essential roles in development and progression of cancers. Multiple regulators, such as phosphatase and tensin homolog (PTEN) and PH domain leucine rich repeat protein phosphatases (PHLPP), have also found to be involved in suppression of the PI3K/Akt signaling pathway. However, how suppressive effects mediated by these regulators are concomitantly disrupted in cancers, which display constitutively activated PI3K/Akt signaling, remains puzzling. In the present study, we reported that the expression of miR-93 was markedly upregulated in glioma cell lines and clinical glioma tissues. Statistical analysis revealed that miR-93 levels significantly correlated with clinicopathologic grade and overall survival in gliomas. Furthermore, we found that overexpressing miR-93 promoted, but inhibition of miR-93 reduced, glioma cell proliferation and cell-cycle progression. We demonstrated that miR-93 activated PI3K/Akt signaling through directly suppressing PTEN, PHLPP2 and FOXO3 expression via targeting their 3’UTRs. Therefore, our results suggest that miR-93 might play an important role in glioma progression and uncover a novel mechanism for constitutive PI3K/Akt activation in gliomas.


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