MiR-200c Inhibits the Tumor Progression of Glioma via Targeting Moesin

Yuanyuan Qin; Weilong Chen; Bingjie Liu; Lei Zhou; Lu Deng; Wanxiang Niu; Dejun Bao; Chuandong Cheng; Dongxue Li; Suling Liu; Chaoshi Niu

doi:10.7150/thno.17886

MiR-200c Inhibits the Tumor Progression of Glioma via Targeting Moesin

Theranostics. 2017 Apr 10;7(6):1663-1673. doi: 10.7150/thno.17886. eCollection 2017.

Authors

Yuanyuan Qin^{1

2

3}, Weilong Chen^{1

2}, Bingjie Liu^{1

2

3}, Lei Zhou^{1

2}, Lu Deng^{1

2}, Wanxiang Niu⁴, Dejun Bao⁴, Chuandong Cheng⁴, Dongxue Li⁴, Suling Liu^{5

6}, Chaoshi Niu^{3

4

7}

Affiliations

¹ The CAS Key Laboratory of Innate Immunity and Chronic Disease, Hefei National Laboratory for Physical Sciences at the Microscale, School of Life Sciences, University of Science and Technology of China, Hefei, Anhui 230027, China.
² Innovation Center for Cell Signaling Network.
³ Medical Center, University of Science and Technology of China, Hefei, Anhui, P.R. China.
⁴ Department of Neurosurgery, Anhui Provincial Hospital Affiliated to Anhui Medical University, Hefei, Anhui 230001, P.R. China.
⁵ Key Laboratory of Breast Cancer in Shanghai, Cancer Institute, Department of Breast Surgery, Fudan University Shanghai Cancer Center, Shanghai 200032, China.
⁶ Institutes of Biomedical Sciences, Fudan University, Shanghai 200032, China.
⁷ AnHui Province Key Laboratory of Brain Function and Brain Disease, Hefei, Anhui 230001, P.R. China.

Abstract

We attempt to demonstrate the regulatory role of miR-200c in glioma progression and its mechanisms behind. Here, we show that miR-200c expression was significantly reduced in the glioma tissues compared to paratumor tissues, especially in malignant glioma. Exogenous overexpression of miR-200c inhibited the proliferation and invasion of glioma cells. In addition, the in vivo mouse xenograft model showed that miR-200c inhibited glioma growth and liver metastasis, which is mainly regulated by targeting moesin (MSN). We demonstrated that the expression of MSN in glioma specimens were negatively correlated with miR-200c expression, and MSN overexpression rescued the phenotype about cell proliferation and invasion induced by miR-200c. Moreover, knockdown of MSN was able to mimic the effects induced by miR-200c in glioma cells. These results indicate that miR-200c plays an important role in the regulation of glioma through targeting MSN.

Keywords: glioma; miR-200c; moesin..

Publication types

Research Support, Non-U.S. Gov't

MeSH terms

Animals
Disease Models, Animal
Glioma / pathology*
Glioma / physiopathology*
Heterografts
Humans
Mice
MicroRNAs / metabolism*
Microfilament Proteins / antagonists & inhibitors*

Substances

MIRN200 microRNA, human
MicroRNAs
Microfilament Proteins
moesin