Inhibitory effects of microRNA-107 on proliferation and in vitro vasculogenic mimicry of Ewing sarcoma cells and the mechanism / 肿瘤
Tumor
; (12): 1282-1288, 2017.
Article
Dans Zh
| WPRIM
| ID: wpr-848446
Responsable en Bibliothèque :
WPRO
ABSTRACT
Objective: To investigate the effects of microRNA-107 (miR-107) on the proliferation and in vitro vasculogenic mimicry of Ewing sarcoma cells, and to explore the possible mechanism. Methods: The expression level of miR-107 in several Ewing sarcoma cell lines was detected by real-time fluorescent quantitative PCR. The synthesized miR-107 mimic and the scramble mimic (as the control) were transfected into Ewing sarcoma RD-ES and SK-ES-1 cells, respectively. The recovery of miR-107 expression in RD-ES and SK-ES-1 cells after transfection was verified by real-time fluorescent quantitative PCR. The effects of miR-107 overexpression on the proliferation and vascular mimicry formation of RD-ES and SK-ES-1 cells were detected by CCK-8 assay and matrigel vasculogenic mimicry assay, respectively. The expressions of hypoxia inducible factor-1ß (HIF-1ß) mRNA and protein in RD-ES and SK-ES-1 cells after transfection with miR-107 mimic were detected by real-time fluorescent quantitative PCR and Western blotting. Results: Comparing with human mesenchymal stem cells, miR-107 was low expressed in Ewing sarcoma RD-ES and SK-ES-1 cells (both P < 0.01). After transfection with miR-107 mimic, the expression of miR-107 was significantly up-regulated in RD-ES and SK-ES-1 cells (both P < 0.01). The proliferation and vascular mimicry formation of RD-ES and SK-ES-1 cells were significantly inhibited after transfection with miR-107 mimic (all P < 0.05). Furthermore, miR-107 overexpression significantly suppressed the expressions of HIF-1ß mRNA and protein in RD-ES and SK-ES-1 cells (all P < 0.01). Conclusion: miR-107 was low-expressed in Ewing sarcoma RD-ES and SK-ES-1 cells. The overexpression of miR-107 can inhibit the proliferation and vascularization of Ewing sarcoma cells, which may be related to the targeting regulation of HIF-1ß expression.
Texte intégral:
1
Indice:
WPRIM
langue:
Zh
Texte intégral:
Tumor
Année:
2017
Type:
Article