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Eur Rev Med Pharmacol Sci ; 23(20): 8806-8812, 2019 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-31696467

RESUMO

OBJECTIVE: Increasing evidence indicated that microRNAs (miRNAs) are crucial regulators for cancer development. Bladder cancer (BCa) is a major threat to human health. The aim of this study was to analyze the roles of miR-652-3p in BCa, and to explore the associated mechanisms. MATERIALS AND METHODS: MiR-652-3p expression in BCa cell lines was explored using Real Time-quantitative Polymerase Chain Reaction (RT-qPCR) method. MiR-652-3p expression level in BCa tissues was explored at StarBase. Cell Counting Kit-8 (CCK-8) assay, wound-healing assay, and transwell invasion assay were conducted to investigate the biological roles of miR-652-3p. The underlying mechanisms of miR-652-3p in NSCLC were investigated using luciferase activity reporter assay and rescue experiments. RESULTS: We showed that miR-652-3p expression level was upregulated in both BCa tissues and cell lines. The knockdown of miR-652-3p significantly inhibited BCa cell proliferation, migration, and invasion in vitro. Moreover, we showed that potassium intermediate/small conductance calcium-activated channel, subfamily N, member 3 (KCNN3) was a functional target for miR-652-3p. Besides, the expression of KCNN3 in BCa tissues was negatively correlated with miR-652-3p. CONCLUSIONS: Collectively, these results showed that miR-652-3p could promote BCa cell proliferation, migration, and invasion via directly regulating KCNN3, which may provide a novel therapeutic target for BCa treatment.


Assuntos
MicroRNAs/metabolismo , Canais de Potássio Ativados por Cálcio de Condutância Baixa/metabolismo , Neoplasias da Bexiga Urinária/patologia , Regiões 3' não Traduzidas , Antagomirs/metabolismo , Sequência de Bases , Sítios de Ligação , Linhagem Celular Tumoral , Movimento Celular , Proliferação de Células , Humanos , MicroRNAs/antagonistas & inibidores , MicroRNAs/genética , Alinhamento de Sequência , Canais de Potássio Ativados por Cálcio de Condutância Baixa/antagonistas & inibidores , Canais de Potássio Ativados por Cálcio de Condutância Baixa/genética , Regulação para Cima , Neoplasias da Bexiga Urinária/genética , Neoplasias da Bexiga Urinária/metabolismo
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