Oncotarget

Research Papers:

MiR-367 regulates cell proliferation and metastasis by targeting metastasis-associated protein 3 (MTA3) in clear-cell renal cell carcinoma

Dexin Ding, Yue Zhang, Lin Wen, Jiangbo Fu, Xue Bai, Yuhua Fan, Yuan Lin, Hongshuang Dai, Qiang Li, Yong Zhang and Ruihua An _

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Oncotarget. 2017; 8:63084-63095. https://doi.org/10.18632/oncotarget.18647

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Abstract

Dexin Ding1,2,*, Yue Zhang3,*, Lin Wen3, Jiangbo Fu3, Xue Bai3, Yuhua Fan4, Yuan Lin3, Hongshuang Dai2, Qiang Li2, Yong Zhang3 and Ruihua An1

1Department of Urology, The First Affiliated Hospital of The Harbin Medical University, Harbin 150001, China

2Department of Urology, The Affiliated Tumor Hospital of The Harbin Medical University, Harbin 150001, China

3Department of Pharmacology, State-Province Key Laboratories of Biomedicine-Pharmaceutics of China, Key Laboratory of Cardiovascular Research, Ministry of Education, College of Pharmacy, Harbin Medical University, Harbin 150081, China

4Department of Biotechnology and Pharmaceutics, College of Pharmacy, Harbin Medical University-Daqing, Daqing 163319, China

*These authors have contributed equally to this work

Correspondence to:

Ruihua An, email: [email protected]

Yong Zhang, email: [email protected]

Keywords: miR-367, MTA3, ccRCC, proliferation, metastasis

Received: March 06, 2017     Accepted: May 22, 2017     Published: June 27, 2017

ABSTRACT

Clear-cell renal cell carcinoma (ccRCC) is an aggressive and malignant kidney cancer which has the worst prognosis. Although microRNAs (miRNAs) have recently been identified as a novel class of regulators in oncogenesis and metastasis, there are few studies on their participation in ccRCC. In the present study, we observed that miR-367 expression was increased in both human ccRCC tissues and cell lines. Cell proliferation was evaluated by MTT assay and 5-Ethynyl-2′-deoxyuridine (EdU) assay kit, which indicated that inhibition of miR-367 could suppress the ccRCC proliferation. Forced expression of miR-367 substantially induced cell migration and invasion evidenced by wound-healing and transwell assays, and this carcinogenesis could be abolished by miR-367 inhibitor treatment. Further analysis identified Metastasis-Associated Protein 3 (MTA3) as a direct target of miR-367. QRT-PCR and western blot results indicated the correlative expression of miR-367 and MTA3 in ccRCC tissue samples. Overexpression of MTA3 reversed miR-367-induced cell proliferation, migration and invasion. Our data uncovered a novel molecular interaction between miR-367 and MTA3, indicating a therapeutic strategy of miR-367 for ccRCC.


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