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Kaohsiung J Med Sci ; 37(1): 20-26, 2021 Jan.
Artigo em Inglês | MEDLINE | ID: mdl-32833340

RESUMO

MicroRNA-3175 (miR-3175) expression is upregulated in prostate cancer, but its roles and the underlying mechanisms in prostate cancer cell growth and invasion need to be elucidated. This study aimed to uncover the roles of miR-3175 in regulating cell growth and migration, as well as the expression of its predicted target gene cardiac sodium channel ß4-subunit gene (SCN4B). Real-time quantitative PCR (RT-qPCR) and/or western blotting techniques were used to measure miR-3175 and SCN4B expression levels in prostate cancer cells. Inhibitor or mimics transfections were used to overexpress or silence miR-3175 in prostate cancer cells. MTT and Edu assays were applied to assess cell viability. Scratch assay and transwell chambers were used to examine cell migration and invasion abilities. The interaction between miR-3175 and SCN4B was determined by means of luciferase gene reporter, RT-qPCR, and western blotting assays. The results showed that miR-3175 expression was increased and SCN4B expression was decreased in prostate cancer cell lines as compared with normal human prostatic epithelial cells. Compared with the control group, knockdown of miR-3175 resulted in strong inhibitions of cell growth, migration, invasion, and N-cadherin expression, together with an increase in E-cadherin expression. In addition, knockdown of miR-3175 dramatically increased the luciferase activity of the luciferase vector of SCN4B, and increased SCN4B expression. Together, this study illustrated that downregulation of miR-3175 repressed the proliferation and invasion of prostate cancer cells, which might be induced by SCN4B downregulation.


Assuntos
Inativação Gênica , MicroRNAs/metabolismo , Neoplasias da Próstata/genética , Neoplasias da Próstata/patologia , Subunidade beta-4 do Canal de Sódio Disparado por Voltagem/genética , Sequência de Bases , Linhagem Celular Tumoral , Movimento Celular/genética , Proliferação de Células/genética , Regulação Neoplásica da Expressão Gênica , Humanos , Masculino , MicroRNAs/genética , Invasividade Neoplásica , Subunidade beta-4 do Canal de Sódio Disparado por Voltagem/metabolismo
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