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Int J Clin Exp Pathol. 2015 May 1;8(5):5224-9. eCollection 2015.

miRNA-221 promotes proliferation, migration and invasion by targeting TIMP2 in renal cell carcinoma.

Author information

1
Clinical Laboratory, The First Affiliated Hospital of Xinxiang Medical University Weihui 453100, China.
2
Blood Transfusion Room, The First Affiliated Hospital of Xinxiang Medical University Weihui 453100, China.
3
Department of Pathology, The First Affiliated Hospital of Xinxiang Medical University Weihui 453100, China.
4
Medical Inspection Institute, Xinxiang Medical University Xinxiang 453000, China.

Abstract

INTRODUCTION:

MicroRNAs (miRNAs) play important roles in tumorigenesis. In this study, we investigated the role of miR-221 in the development and progression of clear cell renal cell carcinoma (ccRCC).

METHODS:

Quantitative real-time PCR (qRT-PCR) was used to measure the expression level of miR-221 in ccRCC tissues and cell lines. Then, we investigated the role of miR-221 to determine its potential roles on renal cancer cell proliferation, migration and invasion in vitro. A luciferase reporter assay was conducted to confirm the target gene of miR-221 and the results were validated in renal cancer cells.

RESULTS:

In the present study, we found that miR-221 was significantly increased in ccRCC tissues and cell lines. Knocked-down expression of miR-221 remarkably inhibited cell proliferation, migration and invasion of renal cancer cells. Moreover, at the molecular level, our results suggested that TIMP2 as a direct target of miR-221 through which miR-221 promoted tumor cell proliferation, migration and invasion.

CONCLUSIONS:

These findings suggested that miR-221 play an oncogenic role in the renal cancer cell proliferation, migration and invasion by directly inhibiting the tumor suppressor TIMP2, indicating miR-221 act as a potential new therapeutic target for the treatment of ccRCC.

KEYWORDS:

Clear cell renal cell carcinoma; TIMP2; miR-221

PMID:
26191221
PMCID:
PMC4503093
[Indexed for MEDLINE]
Free PMC Article

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