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Oncol Rep ; 33(5): 2393-401, 2015 May.
Artigo em Inglês | MEDLINE | ID: mdl-25738254

RESUMO

The phosphoinositide 3-kinase (PI3K)/Akt signaling pathway appears to be a key regulator in cervical carcinogenesis. The phosphatase and tensin homolog deleted on chromosome 10 (PTEN) protein is principally involved in the homeostatic maintenance of PI3K/Akt signaling and PTEN has been identified to play an important role in the occurrence and development of cervical cancer. MicroRNA (miRNA)-494 has been proven to be involved in the carcinogenesis and development of various types of cancer by directly targeting PTEN. However the role, mechanism and clinical significance of miR-494 in cervical cancer have not been further reported. In the present study, we analyzed the expression of miR-494 in -with PTEN expression and clinicopathological data of cervical cancer patients. The results showed that miR-494 expression was significantly upregulated in human cervical cancer cell lines and tissues. miR-494 upregulation was significantly associated with PTEN downregulation, adverse clinicopathological characteristics, poor overall and progression-free survival and poor prognosis. In vitro experiments showed that inhibition of miR-494 suppressed cell proliferation and growth by directly targeting the 3'-untranslated region (3'-UTR) of PTEN mRNA. These findings identified a novel molecular mechanism involved in the regulation of PTEN expression and cervical cancer progression. Results of the present study indicated that miR-494 may have an essential role in the carcinogenesis and progression of cervical cancer and targeting miR-494 may be a promising therapeutic strategy for the treatment of cervical cancer.


Assuntos
Carcinoma/genética , Regulação Neoplásica da Expressão Gênica , MicroRNAs/genética , PTEN Fosfo-Hidrolase/genética , RNA Mensageiro/metabolismo , Neoplasias do Colo do Útero/genética , Regiões 3' não Traduzidas , Adulto , Carcinoma/patologia , Linhagem Celular Tumoral , Proliferação de Células/genética , Regulação para Baixo , Feminino , Células HeLa , Humanos , Estadiamento de Neoplasias , Fosfatidilinositol 3-Quinases/metabolismo , Prognóstico , Proteínas Proto-Oncogênicas c-akt/metabolismo , Reação em Cadeia da Polimerase Via Transcriptase Reversa , Transdução de Sinais , Regulação para Cima , Neoplasias do Colo do Útero/patologia
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