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Effects of miRNA-25 on proliferation of human esophageal squamous-cell carcinoma cell line TE1 / 中国病理生理杂志
Chinese Journal of Pathophysiology ; (12): 1979-1985, 2015.
Artículo en Chino | WPRIM | ID: wpr-479562
ABSTRACT

AIM:

To investigate the effects and mechanisms of microRNA-25 (miRNA-25) on the proliferation of human esophageal squamous-cell carcinoma cell line TE1.

METHODS:

The abundance of miRNA-25 in different tis-sues was measured by RT-PCR.After silencing or over-expression of miRNA-25 with mimics or inhibitor in TE1 cells, the cell proliferation, cell cycle distribution and the expression of cyclin E1 and cyclin-dependent kinase 2 (CDK2) at mRNA and protein levels were measured by CCK-8 assay, BrdU detection, flow cytometry, RT-PCR and Western blot, respective-ly.

RESULTS:

miRNA-25 was prominent in esophageal mucosal tissue and highly expressed in TE1 cells (P<0.05).O-ver-expression of miRNA-25 increased TE1 cell proliferation, promoted the cell cycle progression and enhanced the en-trance of the cells into S phase (P<0.05).Inverse results were obtained after down-regulation of miRNA-25 (P<0.05). Furthermore, the expression of cyclin E1 and CDK2 at mRNA and protein levels was significantly increased after over-ex-pression of miRNA-25, but decreased after down-regulation of miRNA-25 (P<0.05).

CONCLUSION:

miRNA-25 en-hances cell cycle transition by increasing the expression of cyclin E1 and CDK2, thus accelerating TE1 cell proliferation. This study provides a novel mechanism by which miRNA-25 increases the proliferation of human esophageal squamous-cell carcinoma cell line TE1, suggesting that down-regulation of miRNA-25 may be a potential new therapeutic strategy for trea-ting esophageal squamous-cell carcinoma.

Texto completo: Disponible Índice: WPRIM (Pacífico Occidental) Idioma: Chino Revista: Chinese Journal of Pathophysiology Año: 2015 Tipo del documento: Artículo

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Texto completo: Disponible Índice: WPRIM (Pacífico Occidental) Idioma: Chino Revista: Chinese Journal of Pathophysiology Año: 2015 Tipo del documento: Artículo