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Long noncoding RNA LINC01291 promotes the aggressive properties of melanoma by functioning as a competing endogenous RNA for microRNA-625-5p and subsequently increasing IGF-1R expression

Studies have confirmed the relationship between dysregulated long noncoding RNAs and melanoma pathogenesis. However, the regulatory functions of long intergenic non-protein coding RNA 1291 (LINC01291) in melanoma remain unknown. Therefore, we evaluated LINC01291 expression in melanoma and explored i...

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Autores principales: Wu, Lijun, Li, Ke, Lin, Wei, Liu, Jianjiang, Qi, Qiang, Shen, Guoliang, Chen, Weixin, He, Wenjun
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Nature Publishing Group US 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8940622/
https://www.ncbi.nlm.nih.gov/pubmed/33674778
http://dx.doi.org/10.1038/s41417-021-00313-9
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author Wu, Lijun
Li, Ke
Lin, Wei
Liu, Jianjiang
Qi, Qiang
Shen, Guoliang
Chen, Weixin
He, Wenjun
author_facet Wu, Lijun
Li, Ke
Lin, Wei
Liu, Jianjiang
Qi, Qiang
Shen, Guoliang
Chen, Weixin
He, Wenjun
author_sort Wu, Lijun
collection PubMed
description Studies have confirmed the relationship between dysregulated long noncoding RNAs and melanoma pathogenesis. However, the regulatory functions of long intergenic non-protein coding RNA 1291 (LINC01291) in melanoma remain unknown. Therefore, we evaluated LINC01291 expression in melanoma and explored its roles in regulating tumor behaviors. Further, the molecular events via which LINC01291 affects melanoma cells were investigated. LINC01291 expression in melanoma cells was analyzed using The Cancer Genome Atlas database and quantitative real-time polymerase chain reaction. Functional assays, including the Cell Counting Kit-8 assay, colony formation assay, flow cytometry, cell migration and invasion assays, and tumor xenograft models, were used to examine LINC01291’s role in melanoma cells. Additionally, bioinformatics analysis, RNA immunoprecipitation, luciferase reporter assay, and western blotting were conducted to determine the tumor-promoting mechanism of LINC01291. LINC01291 was upregulated in melanoma tissues and cell lines. Following LINC01291 knockdown, cell proliferation, colony formation, migration, and invasion were diminished, whereas apoptosis was enhanced and the cell cycle was arrested at G0/G1. In addition, loss of LINC01291 decreased the chemoresistance of melanoma cells to cisplatin. Furthermore, LINC01291 interference inhibited melanoma tumor growth in vivo. Mechanistically, LINC01291 functions as a competing endogenous RNA by sponging microRNA-625-5p (miR-625-5p) in melanoma cells and maintaining insulin-like growth factor 1 receptor (IGF-1R) expression. Rescue experiments revealed that the roles induced by LINC01291 depletion in melanoma cells could be reversed by suppressing miR-625-5p or overexpressing IGF-1R. Our study identified the LINC01291/miR-625-5p/IGF-1R competing endogenous RNA pathway in melanoma cells, which may represent a novel diagnostic biomarker and an effective therapeutic target for melanoma.
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spelling pubmed-89406222022-04-07 Long noncoding RNA LINC01291 promotes the aggressive properties of melanoma by functioning as a competing endogenous RNA for microRNA-625-5p and subsequently increasing IGF-1R expression Wu, Lijun Li, Ke Lin, Wei Liu, Jianjiang Qi, Qiang Shen, Guoliang Chen, Weixin He, Wenjun Cancer Gene Ther Article Studies have confirmed the relationship between dysregulated long noncoding RNAs and melanoma pathogenesis. However, the regulatory functions of long intergenic non-protein coding RNA 1291 (LINC01291) in melanoma remain unknown. Therefore, we evaluated LINC01291 expression in melanoma and explored its roles in regulating tumor behaviors. Further, the molecular events via which LINC01291 affects melanoma cells were investigated. LINC01291 expression in melanoma cells was analyzed using The Cancer Genome Atlas database and quantitative real-time polymerase chain reaction. Functional assays, including the Cell Counting Kit-8 assay, colony formation assay, flow cytometry, cell migration and invasion assays, and tumor xenograft models, were used to examine LINC01291’s role in melanoma cells. Additionally, bioinformatics analysis, RNA immunoprecipitation, luciferase reporter assay, and western blotting were conducted to determine the tumor-promoting mechanism of LINC01291. LINC01291 was upregulated in melanoma tissues and cell lines. Following LINC01291 knockdown, cell proliferation, colony formation, migration, and invasion were diminished, whereas apoptosis was enhanced and the cell cycle was arrested at G0/G1. In addition, loss of LINC01291 decreased the chemoresistance of melanoma cells to cisplatin. Furthermore, LINC01291 interference inhibited melanoma tumor growth in vivo. Mechanistically, LINC01291 functions as a competing endogenous RNA by sponging microRNA-625-5p (miR-625-5p) in melanoma cells and maintaining insulin-like growth factor 1 receptor (IGF-1R) expression. Rescue experiments revealed that the roles induced by LINC01291 depletion in melanoma cells could be reversed by suppressing miR-625-5p or overexpressing IGF-1R. Our study identified the LINC01291/miR-625-5p/IGF-1R competing endogenous RNA pathway in melanoma cells, which may represent a novel diagnostic biomarker and an effective therapeutic target for melanoma. Nature Publishing Group US 2021-03-05 2022 /pmc/articles/PMC8940622/ /pubmed/33674778 http://dx.doi.org/10.1038/s41417-021-00313-9 Text en © The Author(s), under exclusive licence to Springer Nature America, Inc. part of Springer Nature 2021 https://creativecommons.org/licenses/by/4.0/Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) .
spellingShingle Article
Wu, Lijun
Li, Ke
Lin, Wei
Liu, Jianjiang
Qi, Qiang
Shen, Guoliang
Chen, Weixin
He, Wenjun
Long noncoding RNA LINC01291 promotes the aggressive properties of melanoma by functioning as a competing endogenous RNA for microRNA-625-5p and subsequently increasing IGF-1R expression
title Long noncoding RNA LINC01291 promotes the aggressive properties of melanoma by functioning as a competing endogenous RNA for microRNA-625-5p and subsequently increasing IGF-1R expression
title_full Long noncoding RNA LINC01291 promotes the aggressive properties of melanoma by functioning as a competing endogenous RNA for microRNA-625-5p and subsequently increasing IGF-1R expression
title_fullStr Long noncoding RNA LINC01291 promotes the aggressive properties of melanoma by functioning as a competing endogenous RNA for microRNA-625-5p and subsequently increasing IGF-1R expression
title_full_unstemmed Long noncoding RNA LINC01291 promotes the aggressive properties of melanoma by functioning as a competing endogenous RNA for microRNA-625-5p and subsequently increasing IGF-1R expression
title_short Long noncoding RNA LINC01291 promotes the aggressive properties of melanoma by functioning as a competing endogenous RNA for microRNA-625-5p and subsequently increasing IGF-1R expression
title_sort long noncoding rna linc01291 promotes the aggressive properties of melanoma by functioning as a competing endogenous rna for microrna-625-5p and subsequently increasing igf-1r expression
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8940622/
https://www.ncbi.nlm.nih.gov/pubmed/33674778
http://dx.doi.org/10.1038/s41417-021-00313-9
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