MicroRNA-126 inhibits tumor cell invasion and metastasis by downregulating ROCK1 in renal cell carcinoma.
Mol Med Rep
; 13(6): 5029-2036, 2016 Jun.
Article
en En
| MEDLINE
| ID: mdl-27108693
MicroRNAs (miRNAs) are involved in cancer development and progression. Renal cell carcinoma (RCC) frequently undergoes metastasis and has a high mortality rate. The current study measured miRNA126 (miR126) expression levels in 128 pairs of clear cell RCC and adjacent normal kidney tissue samples by reverse transcriptionquantitative polymerase chain reaction, and analyzed the association between miR126 and various clinicopathological parameters. In addition, cell proliferation, wound healing and cell invasion assays were conducted using RCC cells overexpressing miR126. Potential miR126 target genes and the signaling pathways that may be regulated by miR126 were then examined. miR126 expression was significantly reduced in patients with metastatic RCC compared with patients without metastasis. Consistently, overexpression of miR126 in RCC cells significantly inhibited cell proliferation, migration and invasion in vitro compared with negative control miRNA. A luciferase reporter assay demonstrated that miR126 targets Rho associated coiledcoil containing protein kinase 1 (ROCK1) by directly binding the 3'untranslated region. Furthermore, western blotting identified miR126 as an important regulator of the AKT and extracellular signalregulated 1/2 signaling pathways. The results of the present study indicate that miR126 inhibits RCC cell proliferation, migration and invasion by downregulating ROCK1. These findings suggest that miR126 may be valuable as a potential target for therapeutic intervention in RCC.
Texto completo:
1
Banco de datos:
MEDLINE
Asunto principal:
Carcinoma de Células Renales
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Regulación Neoplásica de la Expresión Génica
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MicroARNs
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Interferencia de ARN
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Quinasas Asociadas a rho
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Neoplasias Renales
Tipo de estudio:
Diagnostic_studies
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Prognostic_studies
Límite:
Aged
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Aged80
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Female
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Humans
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Male
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Middle aged
Idioma:
En
Revista:
Mol Med Rep
Año:
2016
Tipo del documento:
Article