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Hsa-miR-3658 Promotes Cell Proliferation, Migration and Invasion by Effecting LASS2 in Bladder Cancer.
Clin Lab ; 64(4): 515-525, 2018 Apr 01.
Article em En | MEDLINE | ID: mdl-29739079
BACKGROUND: Hsa-miR-3658 is upregulated in various tumors, but its expression in bladder cancer has been rarely studied. METHODS: In this study, hsa-miR-3658 expressions in several bladder cancer cell lines were examined, and its effect on the malignant degree of bladder cancer and whether hsa-miR-3658 regulates tumor biological behaviors through LASS2 and its downstream molecular pathway were studied and validated. RESULTS: It was found miR-3658 expressions differed among different cell lines, which may be an influence factor on the malignancy. MiR-3658 can enhance the proliferation, migration and invasion of bladder cancer cells, inhibit cell adhesion and reduce cell chemosensitivity. MiR-3658 can promote the epithelial-mesenchymal transition of bladder cancer cells through the molecular mechanism of affecting the expressions of epithelial-mesenchymal transition marker protein and related transcription factors. CONCLUSIONS: MiRNA-3658 is upregulated in bladder cancer cells, and this change is associated with the proliferation, invasion and resistance of bladder cancer cells. The effect of miR-3658 on bladder cancer cell biology may be associated with the effect on LASS2.
Assuntos

Texto completo: 1 Base de dados: MEDLINE Assunto principal: Neoplasias da Bexiga Urinária / Regulação Neoplásica da Expressão Gênica / Movimento Celular / Proteínas Supressoras de Tumor / MicroRNAs / Proliferação de Células / Esfingosina N-Aciltransferase / Proteínas de Membrana Limite: Humans Idioma: En Ano de publicação: 2018 Tipo de documento: Article

Texto completo: 1 Base de dados: MEDLINE Assunto principal: Neoplasias da Bexiga Urinária / Regulação Neoplásica da Expressão Gênica / Movimento Celular / Proteínas Supressoras de Tumor / MicroRNAs / Proliferação de Células / Esfingosina N-Aciltransferase / Proteínas de Membrana Limite: Humans Idioma: En Ano de publicação: 2018 Tipo de documento: Article