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Effect of miR-21 on the proliferation and migration of human hepatoma BEL-7402 cells through AKT/ERK pathway / 肿瘤
Tumor ; (12): 947-953, 2013.
Artículo en Chino | WPRIM | ID: wpr-848932
ABSTRACT

Objective:

To investigate the effects of miR-21 on the proliferation, invasion and migration of human hepatoma BEL-7402 cells and explore the possible mechanism.

Methods:

MiR-21 over-expression vector pGL3-miR21-EGFP (enhanced green fluorescent protein) was transfected into BEL-7402 cells. The expression level of miR-21 was detected by real-time fluorescence quantitative-PCR and the expression levels of phospho-AKT (p-AKT) and phospho-extracellular signal response kinase (p-ERK) were detected by Western blotting. The cell viability was examined by MTT assay. The cell migration and invasion abilities were evaluated by wound-healing assay and Transwell assay, respectively. The pGenesil-shAKT was transfected into BEL-7401 cells, and then the expression level of miR-21 was detected by real-time fluorescence quantitative-PCR, the expression levels of AKT and p-AKT were detected by Western blotting, the cell viability was examined by MTT assay, and the cell migration ability was evaluated by wound-healing assay.

Results:

As compared with the blank control (without transfection), the expression levels of miR-21 (P < 0.01), p-AKT and p-ERK (both P < 0.05) were up-regulated in BEL-7402 cells after transfection with pGL3-miR21-EGFP. As compared with the blank control, over-expression of miR-21 significantly promoted the proliferation, migration and invasion of BEL-7402 cells (all P < 0.05). After transfection with pGenesil-shAKT vector, the expression levels of AKT and p-AKT were down-regulated and the proliferation and migration abilities of BEL-7402 cells were inhibited (P < 0.05), but the expression level of miR-21 had no significant change.

Conclusion:

MiR-21 may contribute to the enhancement of proliferation and migration abilities of BEL-7402 cells through AKT/ERK signal pathway. Copyright © 2013 by TUMOR.

Texto completo: Disponible Índice: WPRIM (Pacífico Occidental) Idioma: Chino Revista: Tumor Año: 2013 Tipo del documento: Artículo

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Texto completo: Disponible Índice: WPRIM (Pacífico Occidental) Idioma: Chino Revista: Tumor Año: 2013 Tipo del documento: Artículo