Long non-coding RNA BANCR promotes proliferation in malignant melanoma by regulating MAPK pathway activation.

Long non-coding RNAs (lncRNAs) have been shown to be implicated in the complex network of cancer including malignant melanoma and play important roles in tumorigenesis and progression. However, their functions and downstream mechanisms are largely unknown. This study aimed to investigate whether BRA...

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Autores principales:	Ruiya Li, Lingli Zhang, Lizhou Jia, Yan Duan, Yan Li, Lidao Bao, Na Sha
Formato:	article
Lenguaje:	EN
Publicado:	Public Library of Science (PLoS) 2014
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/c0dc1684c6534cb1a69132de4e734cf6
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spelling	oai:doaj.org-article:c0dc1684c6534cb1a69132de4e734cf62021-11-11T08:21:27ZLong non-coding RNA BANCR promotes proliferation in malignant melanoma by regulating MAPK pathway activation.1932-620310.1371/journal.pone.0100893https://doaj.org/article/c0dc1684c6534cb1a69132de4e734cf62014-01-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/24967732/?tool=EBIhttps://doaj.org/toc/1932-6203Long non-coding RNAs (lncRNAs) have been shown to be implicated in the complex network of cancer including malignant melanoma and play important roles in tumorigenesis and progression. However, their functions and downstream mechanisms are largely unknown. This study aimed to investigate whether BRAF-activated non-coding RNA (BANCR), a novel and potential regulator of melanoma cell, participates in the proliferation of malignant melanoma and elucidate the underlying mechanism in this process. We found that BANCR was abnormally overexpressed in human malignant melanoma cell lines and tissues, and increased with tumor stages by quantitative PCR. BANCR knockdown induced by shRNA transfection significantly inhibited proliferation of tumor cells and inactivated MAPK pathway, especially by silencing the ERK1/2 and JNK component. Moreover, combination treatment of BANCR knockdown and suppression ERK1/2 or JNK (induced by specific inhibitors U0126 or SP600125 respectively) produced synergistic inhibitory effects in vitro. And the inhibitory effects induced by ERK1/2 or JNK could be rescued by BANCR overexpression. By tumorigenicity assay in BALB/c nude mice, we further found that BANCR knockdown inhibited tumor growth in vivo. In addition, patients with high expression of BANCR had a lower survival rate. Taken together, we confirmed the abnormal upregulation of a novel lncRNA, BANCR, in human malignant melanoma. BANCR was involved in melanoma cell proliferation both in vitro and in vivo. The linkage between BANCR and MAPK pathway may provide a novel interpretation for the mechanism of proliferation regulation in malignant melanoma.Ruiya LiLingli ZhangLizhou JiaYan DuanYan LiLidao BaoNa ShaPublic Library of Science (PLoS)articleMedicineRScienceQENPLoS ONE, Vol 9, Iss 6, p e100893 (2014)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Ruiya Li Lingli Zhang Lizhou Jia Yan Duan Yan Li Lidao Bao Na Sha Long non-coding RNA BANCR promotes proliferation in malignant melanoma by regulating MAPK pathway activation.
description	Long non-coding RNAs (lncRNAs) have been shown to be implicated in the complex network of cancer including malignant melanoma and play important roles in tumorigenesis and progression. However, their functions and downstream mechanisms are largely unknown. This study aimed to investigate whether BRAF-activated non-coding RNA (BANCR), a novel and potential regulator of melanoma cell, participates in the proliferation of malignant melanoma and elucidate the underlying mechanism in this process. We found that BANCR was abnormally overexpressed in human malignant melanoma cell lines and tissues, and increased with tumor stages by quantitative PCR. BANCR knockdown induced by shRNA transfection significantly inhibited proliferation of tumor cells and inactivated MAPK pathway, especially by silencing the ERK1/2 and JNK component. Moreover, combination treatment of BANCR knockdown and suppression ERK1/2 or JNK (induced by specific inhibitors U0126 or SP600125 respectively) produced synergistic inhibitory effects in vitro. And the inhibitory effects induced by ERK1/2 or JNK could be rescued by BANCR overexpression. By tumorigenicity assay in BALB/c nude mice, we further found that BANCR knockdown inhibited tumor growth in vivo. In addition, patients with high expression of BANCR had a lower survival rate. Taken together, we confirmed the abnormal upregulation of a novel lncRNA, BANCR, in human malignant melanoma. BANCR was involved in melanoma cell proliferation both in vitro and in vivo. The linkage between BANCR and MAPK pathway may provide a novel interpretation for the mechanism of proliferation regulation in malignant melanoma.
format	article
author	Ruiya Li Lingli Zhang Lizhou Jia Yan Duan Yan Li Lidao Bao Na Sha
author_facet	Ruiya Li Lingli Zhang Lizhou Jia Yan Duan Yan Li Lidao Bao Na Sha
author_sort	Ruiya Li
title	Long non-coding RNA BANCR promotes proliferation in malignant melanoma by regulating MAPK pathway activation.
title_short	Long non-coding RNA BANCR promotes proliferation in malignant melanoma by regulating MAPK pathway activation.
title_full	Long non-coding RNA BANCR promotes proliferation in malignant melanoma by regulating MAPK pathway activation.
title_fullStr	Long non-coding RNA BANCR promotes proliferation in malignant melanoma by regulating MAPK pathway activation.
title_full_unstemmed	Long non-coding RNA BANCR promotes proliferation in malignant melanoma by regulating MAPK pathway activation.
title_sort	long non-coding rna bancr promotes proliferation in malignant melanoma by regulating mapk pathway activation.
publisher	Public Library of Science (PLoS)
publishDate	2014
url	https://doaj.org/article/c0dc1684c6534cb1a69132de4e734cf6
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Long non-coding RNA BANCR promotes proliferation in malignant melanoma by regulating MAPK pathway activation.

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