Oncotarget

Research Papers:

This article has been corrected. Correction in: Oncotarget. 2017; 8:60723.

MiR-34a-5p promotes the multi-drug resistance of osteosarcoma by targeting the CD117 gene

Youguang Pu _, Fangfang Zhao, Haiyan Wang, Wenjing Cai, Jin Gao, Yinpeng Li and Shanbao Cai

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Oncotarget. 2016; 7:28420-28434. https://doi.org/10.18632/oncotarget.8546

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Abstract

Shanbao Cai1,6,*, Youguang Pu1,*, Fangfang Zhao1,*, Haiyan Wang2, Wenjing Cai3, Jin Gao4 and Yinpeng Li5

1Cancer Epigenetics Program, Anhui Cancer Hospital, West District of Anhui Provincial Hospital, Hefei 230031, Anhui, China

2Department of Clinical Geriatrics, Anhui Provincial Hospital, Hefei 230031, Anhui, China

3Indiana University School of Medicine, Indianapolis, IN 46202, USA

4Department of Radiation Oncology, Anhui Cancer Hospital, West District of Anhui Provincial Hospital, Hefei 230031, Anhui, China

5Xinxiang Medical University, Xinxiang 453000, Henan, China

6Department of Orthopedic Surgery, Anhui Cancer Hospital, West District of Anhui Provincial Hospital, Hefei 230031, Anhui, China

*These authors have contributed equally to this work

Correspondence to:

Shanbao Cai, email: [email protected]

Keywords: miR-34a-5p, CD117, multi-drug resistance, osteosarcoma

Received: July 03, 2015     Accepted: March 06, 2016     Published: April 1, 2016

ABSTRACT

An association has been reported between miR-34a-5p and several types of cancer. Specifically, in this study, using systematic observations of multi-drug sensitive (G-292 and MG63.2) and resistant (SJSA-1 and MNNG/HOS) osteosarcoma (OS) cell lines, we showed that miR-34a-5p promotes the multi-drug resistance of OS through the receptor tyrosine kinase CD117, a direct target of miR-34a-5p. Consistently, the siRNA-mediated repression of CD117 in G-292 and MG63.2 cells led to a similar phenotype that exhibited all of the miR-34a-5p mimic-triggered changes. In addition, the activity of the MEF2 signaling pathway was drastically altered by the forced changes in the miR-34a-5p or CD117 level in OS cells. Furthermore, si-CD117 suppressed the enhanced colony and sphere formation, which is in agreement with the characteristics of a cancer stem marker. Taken together, our data established CD117 as a direct target of miR-34-5p and demonstrated that this regulation interferes with several CD117-mediated effects on OS cells. In addition to providing new mechanistic insights, our results will provide an approach for diagnosing and chemotherapeutically treating OS.


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