MicroRNA-4530 promotes angiogenesis by targeting VASH1 in breast carcinoma cells

MicroRNA-4530 通过靶向乳腺癌细胞中的 VASH1 促进血管生成

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作者:Tao Zhang, Li Jing, Hong Li, Linchao Ding, Dongdong Ai, Jianxin Lyu, Lianjin Zhong

Abstract

The results of our previous study revealed that microRNA (miRNA/miR)-4530 was upregulated in the serum of patients with diabetic retinopathy. The TargetScan miRNA database was used to identify potential targets of miR-4530 and vasohibin-1 (VASH1) was predicted as one of the targets. The results of our previous study demonstrated that miR-4530 was able to promote angiogenesis in human umbilical vein endothelial cells. Therefore, suppressing miR-4530 may be a potentially novel approach towards inhibiting tumor angiogenesis. The present study aimed to investigate the function of miR-4530 and determine whether miR-4530 was able to regulate angiogenesis in breast carcinoma cells by targeting VASH1. MDA-MB-231 and MCF-7 cells were transfected with miR-4530 precursor, anti-miR-4530 and empty vector plasmids. The expression levels of miRNA and mRNA were detected using the reverse transcription-quantitative polymerase chain reaction (RT-qPCR). The expression levels of protein were detected using western blotting. Dual-luciferase reporter assays were used to identify the target of miR-4530. Furthermore, cell proliferation, cell cycle, apoptosis and tube formation assays were used to investigate the function of miR-4530 in vitro. Nude mice were used in a subcutaneous tumor model in vivo study. The results of the present study demonstrated that miR-4530 significantly suppressed proliferation and promoted apoptosis of breast carcinoma cells. In addition, miR-4530 expression promoted angiogenesis in vitro. Results from the western blotting and RT-qPCR revealed that VASH1 was significantly downregulated by miR-4530 in breast carcinoma cells. The results of the present study suggest that miR-4530 promotes angiogenesis, inhibits proliferation and induces apoptosis in breast carcinoma cells by suppressing the expression of VASH1.

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