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Long intergenic non-protein coding RNA 511 promotes the progression of osteosarcoma cells through sponging microRNA 618 to upregulate the expression of maelstrom

Osteosarcoma is a tumor disease that commonly exists among young populations. Our research explored the role of the LINC00511/microRNA-618/MAEL axis in osteosarcoma. Expression profiles of long non-coding RNAs (lncRNAs) in osteosarcoma (OS) tissues were constructed, and LINC00511 expression levels w...

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Autores principales: Guo, Wen, Yu, Qing, Zhang, Ming, Li, Fang, Liu, Yu, Jiang, Weiwei, Jiang, Haitao, Li, Haijun
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Impact Journals 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6710040/
https://www.ncbi.nlm.nih.gov/pubmed/31386627
http://dx.doi.org/10.18632/aging.102109
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author Guo, Wen
Yu, Qing
Zhang, Ming
Li, Fang
Liu, Yu
Jiang, Weiwei
Jiang, Haitao
Li, Haijun
author_facet Guo, Wen
Yu, Qing
Zhang, Ming
Li, Fang
Liu, Yu
Jiang, Weiwei
Jiang, Haitao
Li, Haijun
author_sort Guo, Wen
collection PubMed
description Osteosarcoma is a tumor disease that commonly exists among young populations. Our research explored the role of the LINC00511/microRNA-618/MAEL axis in osteosarcoma. Expression profiles of long non-coding RNAs (lncRNAs) in osteosarcoma (OS) tissues were constructed, and LINC00511 expression levels were verified with qRT-PCR. LncRNA-miRNA and miRNA-mRNA interactions were predicted. Validation was performed using a dual-luciferase reporter assay. Protein expression levels of MAEL were evaluated by Western blot assays. The effects of LINC00511, miR-618 and MAEL on the proliferation, viability, and metastasis of OS cells were detected using colony formation, cell counting kit-8 (CCK-8) and transwell assays, respectively. The apoptosis rates of OS cells were investigated using flow cytometry. The tumor-suppressing effect of LINC00511 silencing was also analyzed using a xenograft model in nude mice. LINC00511 overexpression was observed in OS tissues and cell lines. Knockdown of LINC00511 in nude mice inhibited the tumorigenic ability of OS cells. Transfection-induced overexpression of LINC00511 and MAEL, as well as downregulation, highlighted the features of tumor cells, and LINC00511 overexpression reduced apoptosis in vitro. LINC00511 was confirmed to be beneficial for osteosarcoma development via sponging miR-618 and increasing MAEL expression and may thus be considered a potential target for osteosarcoma therapy.
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spelling pubmed-67100402019-09-05 Long intergenic non-protein coding RNA 511 promotes the progression of osteosarcoma cells through sponging microRNA 618 to upregulate the expression of maelstrom Guo, Wen Yu, Qing Zhang, Ming Li, Fang Liu, Yu Jiang, Weiwei Jiang, Haitao Li, Haijun Aging (Albany NY) Research Paper Osteosarcoma is a tumor disease that commonly exists among young populations. Our research explored the role of the LINC00511/microRNA-618/MAEL axis in osteosarcoma. Expression profiles of long non-coding RNAs (lncRNAs) in osteosarcoma (OS) tissues were constructed, and LINC00511 expression levels were verified with qRT-PCR. LncRNA-miRNA and miRNA-mRNA interactions were predicted. Validation was performed using a dual-luciferase reporter assay. Protein expression levels of MAEL were evaluated by Western blot assays. The effects of LINC00511, miR-618 and MAEL on the proliferation, viability, and metastasis of OS cells were detected using colony formation, cell counting kit-8 (CCK-8) and transwell assays, respectively. The apoptosis rates of OS cells were investigated using flow cytometry. The tumor-suppressing effect of LINC00511 silencing was also analyzed using a xenograft model in nude mice. LINC00511 overexpression was observed in OS tissues and cell lines. Knockdown of LINC00511 in nude mice inhibited the tumorigenic ability of OS cells. Transfection-induced overexpression of LINC00511 and MAEL, as well as downregulation, highlighted the features of tumor cells, and LINC00511 overexpression reduced apoptosis in vitro. LINC00511 was confirmed to be beneficial for osteosarcoma development via sponging miR-618 and increasing MAEL expression and may thus be considered a potential target for osteosarcoma therapy. Impact Journals 2019-08-06 /pmc/articles/PMC6710040/ /pubmed/31386627 http://dx.doi.org/10.18632/aging.102109 Text en Copyright © 2019 Guo et al. http://creativecommons.org/licenses/by/3.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution (CC BY) 3.0 License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
spellingShingle Research Paper
Guo, Wen
Yu, Qing
Zhang, Ming
Li, Fang
Liu, Yu
Jiang, Weiwei
Jiang, Haitao
Li, Haijun
Long intergenic non-protein coding RNA 511 promotes the progression of osteosarcoma cells through sponging microRNA 618 to upregulate the expression of maelstrom
title Long intergenic non-protein coding RNA 511 promotes the progression of osteosarcoma cells through sponging microRNA 618 to upregulate the expression of maelstrom
title_full Long intergenic non-protein coding RNA 511 promotes the progression of osteosarcoma cells through sponging microRNA 618 to upregulate the expression of maelstrom
title_fullStr Long intergenic non-protein coding RNA 511 promotes the progression of osteosarcoma cells through sponging microRNA 618 to upregulate the expression of maelstrom
title_full_unstemmed Long intergenic non-protein coding RNA 511 promotes the progression of osteosarcoma cells through sponging microRNA 618 to upregulate the expression of maelstrom
title_short Long intergenic non-protein coding RNA 511 promotes the progression of osteosarcoma cells through sponging microRNA 618 to upregulate the expression of maelstrom
title_sort long intergenic non-protein coding rna 511 promotes the progression of osteosarcoma cells through sponging microrna 618 to upregulate the expression of maelstrom
topic Research Paper
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6710040/
https://www.ncbi.nlm.nih.gov/pubmed/31386627
http://dx.doi.org/10.18632/aging.102109
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