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MiR-219-5p Inhibits the Growth and Metastasis of Malignant Melanoma by Targeting BCL-2

Malignant melanoma is a very dangerous tumor which is resistant to conventional therapy. MicroRNA exerts a vital function in promoting or inhibiting tumor development. The research has investigated the expression and function of miR-219-5p in melanoma. As a result, miR-219-5p expression was distinct...

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Detalles Bibliográficos
Autores principales: Long, Jianwen, Menggen, Qiqige, Wuren, Qimige, Shi, Quan, Pi, Xianming
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Hindawi 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5572586/
https://www.ncbi.nlm.nih.gov/pubmed/28884131
http://dx.doi.org/10.1155/2017/9032502
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author Long, Jianwen
Menggen, Qiqige
Wuren, Qimige
Shi, Quan
Pi, Xianming
author_facet Long, Jianwen
Menggen, Qiqige
Wuren, Qimige
Shi, Quan
Pi, Xianming
author_sort Long, Jianwen
collection PubMed
description Malignant melanoma is a very dangerous tumor which is resistant to conventional therapy. MicroRNA exerts a vital function in promoting or inhibiting tumor development. The research has investigated the expression and function of miR-219-5p in melanoma. As a result, miR-219-5p expression was distinctly reduced in melanoma tissues and cell lines and was negatively correlated with Bcl-2 protein level in melanoma. Patients with low miR-219-5p level represented obviously a low overall survival in comparison with patients with high miR-219-5p level. The upregulation of miR-219-5p inhibited melanoma growth and metastasis and strengthened melanoma cells chemosensitivity by targeting Bcl-2. Therefore, the modulation of miR-219-5p expression may be a novel treatment strategy in melanoma.
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spelling pubmed-55725862017-09-07 MiR-219-5p Inhibits the Growth and Metastasis of Malignant Melanoma by Targeting BCL-2 Long, Jianwen Menggen, Qiqige Wuren, Qimige Shi, Quan Pi, Xianming Biomed Res Int Research Article Malignant melanoma is a very dangerous tumor which is resistant to conventional therapy. MicroRNA exerts a vital function in promoting or inhibiting tumor development. The research has investigated the expression and function of miR-219-5p in melanoma. As a result, miR-219-5p expression was distinctly reduced in melanoma tissues and cell lines and was negatively correlated with Bcl-2 protein level in melanoma. Patients with low miR-219-5p level represented obviously a low overall survival in comparison with patients with high miR-219-5p level. The upregulation of miR-219-5p inhibited melanoma growth and metastasis and strengthened melanoma cells chemosensitivity by targeting Bcl-2. Therefore, the modulation of miR-219-5p expression may be a novel treatment strategy in melanoma. Hindawi 2017 2017-08-13 /pmc/articles/PMC5572586/ /pubmed/28884131 http://dx.doi.org/10.1155/2017/9032502 Text en Copyright © 2017 Jianwen Long et al. https://creativecommons.org/licenses/by/4.0/ This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Research Article
Long, Jianwen
Menggen, Qiqige
Wuren, Qimige
Shi, Quan
Pi, Xianming
MiR-219-5p Inhibits the Growth and Metastasis of Malignant Melanoma by Targeting BCL-2
title MiR-219-5p Inhibits the Growth and Metastasis of Malignant Melanoma by Targeting BCL-2
title_full MiR-219-5p Inhibits the Growth and Metastasis of Malignant Melanoma by Targeting BCL-2
title_fullStr MiR-219-5p Inhibits the Growth and Metastasis of Malignant Melanoma by Targeting BCL-2
title_full_unstemmed MiR-219-5p Inhibits the Growth and Metastasis of Malignant Melanoma by Targeting BCL-2
title_short MiR-219-5p Inhibits the Growth and Metastasis of Malignant Melanoma by Targeting BCL-2
title_sort mir-219-5p inhibits the growth and metastasis of malignant melanoma by targeting bcl-2
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5572586/
https://www.ncbi.nlm.nih.gov/pubmed/28884131
http://dx.doi.org/10.1155/2017/9032502
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