Overexpression of microRNA-497 suppresses cell proliferation and induces apoptosis through targeting paired box 2 in human ovarian cancer.
Oncol Rep
; 36(4): 2101-7, 2016 Oct.
Article
en En
| MEDLINE
| ID: mdl-27513319
ABSTRACT
MicroRNAs are a class of endogenous, small non-coding RNAs which are tightly involved in evolution and progression of human cancers. MicroRNA-497 has been reported as tumor-suppressor in various human cancer. However, the role of miR-497 in ovarian cancer is still poorly known. We investigated the expression level and cellular function of miR-497 in human ovarian cancer. In this study, the expression of miR-497 in ovarian cancer tissues and SKOV3 cells was detected by quantitative reversetranscription polymerase chain reaction (qRT-PCR). CCK-8 assay was used to analysis the cell proliferation. Transwell assay was performed to analysis cell migration and invasion. Cell apoptosis was evaluated by flow cytometry. Luciferase assay was performed to verify a putative target site of miR-497 in the 3'UTR of PAX2 mRNA. The results showed that miR-497 was markedly decreased in ovarian cancer tissues and SKOV3 cells. Moreover, overexpression of miR-497 in SKOV3 cells induced PAX2 protein expression and resulted in inhibition of cell proliferation, migration and invasion, and induction of cell apoptosis. In addition, we confirmed that PAX2 is a direct target gene of miR-497. Furthermore, Silencing of PAX2 by RNA interference suppressed cell proliferation and promoted cell apoptosis in vitro. Taken together, our study rationally present that miR-497 has a potential role as a useful diagnostic and therapeutic biomarker for human ovarian cancer.
Texto completo:
1
Colección:
01-internacional
Base de datos:
MEDLINE
Contexto en salud:
6_ODS3_enfermedades_notrasmisibles
Problema de salud:
6_endocrine_disorders
/
6_ovary_cancer
Asunto principal:
Neoplasias Ováricas
/
Carcinoma
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Apoptosis
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MicroARNs
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Factor de Transcripción PAX2
Límite:
Female
/
Humans
Idioma:
En
Revista:
Oncol Rep
Asunto de la revista:
NEOPLASIAS
Año:
2016
Tipo del documento:
Article