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

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 o...

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Autores principales: Zhang, Tao, Jing, Li, Li, Hong, Ding, Linchao, Ai, Dongdong, Lyu, Jianxin, Zhong, Lianjin
Formato: Online Artículo Texto
Lenguaje:English
Publicado: D.A. Spandidos 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5494889/
https://www.ncbi.nlm.nih.gov/pubmed/28693142
http://dx.doi.org/10.3892/ol.2017.6102
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author Zhang, Tao
Jing, Li
Li, Hong
Ding, Linchao
Ai, Dongdong
Lyu, Jianxin
Zhong, Lianjin
author_facet Zhang, Tao
Jing, Li
Li, Hong
Ding, Linchao
Ai, Dongdong
Lyu, Jianxin
Zhong, Lianjin
author_sort Zhang, Tao
collection PubMed
description 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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spelling pubmed-54948892017-07-07 MicroRNA-4530 promotes angiogenesis by targeting VASH1 in breast carcinoma cells Zhang, Tao Jing, Li Li, Hong Ding, Linchao Ai, Dongdong Lyu, Jianxin Zhong, Lianjin Oncol Lett Articles 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. D.A. Spandidos 2017-07 2017-04-28 /pmc/articles/PMC5494889/ /pubmed/28693142 http://dx.doi.org/10.3892/ol.2017.6102 Text en Copyright: © Zhang et al. This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License (https://creativecommons.org/licenses/by-nc-nd/4.0/) , which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.
spellingShingle Articles
Zhang, Tao
Jing, Li
Li, Hong
Ding, Linchao
Ai, Dongdong
Lyu, Jianxin
Zhong, Lianjin
MicroRNA-4530 promotes angiogenesis by targeting VASH1 in breast carcinoma cells
title MicroRNA-4530 promotes angiogenesis by targeting VASH1 in breast carcinoma cells
title_full MicroRNA-4530 promotes angiogenesis by targeting VASH1 in breast carcinoma cells
title_fullStr MicroRNA-4530 promotes angiogenesis by targeting VASH1 in breast carcinoma cells
title_full_unstemmed MicroRNA-4530 promotes angiogenesis by targeting VASH1 in breast carcinoma cells
title_short MicroRNA-4530 promotes angiogenesis by targeting VASH1 in breast carcinoma cells
title_sort microrna-4530 promotes angiogenesis by targeting vash1 in breast carcinoma cells
topic Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5494889/
https://www.ncbi.nlm.nih.gov/pubmed/28693142
http://dx.doi.org/10.3892/ol.2017.6102
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