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MALAT1 promotes proliferation, migration, and invasion of MG63 cells by upregulation of TGIF2 via negatively regulating miR-129

PURPOSE: This article aimed to investigate the mechanism by which MALAT1 and miR-129 affected the development of osteosarcoma. METHODS: Tumor tissues and adjacent tissues of 23 osteosarcoma patients were collected. Normal osteoblasts hFOB1.19 and osteosarcoma cells MG63 were cultured. MG63 cells wer...

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Detalles Bibliográficos
Autores principales: Liu, Kai, Zhang, Yingang, Liu, Liang, Yuan, Qiling
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Dove Medical Press 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6287664/
https://www.ncbi.nlm.nih.gov/pubmed/30584331
http://dx.doi.org/10.2147/OTT.S182993
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author Liu, Kai
Zhang, Yingang
Liu, Liang
Yuan, Qiling
author_facet Liu, Kai
Zhang, Yingang
Liu, Liang
Yuan, Qiling
author_sort Liu, Kai
collection PubMed
description PURPOSE: This article aimed to investigate the mechanism by which MALAT1 and miR-129 affected the development of osteosarcoma. METHODS: Tumor tissues and adjacent tissues of 23 osteosarcoma patients were collected. Normal osteoblasts hFOB1.19 and osteosarcoma cells MG63 were cultured. MG63 cells were transfected and grouped: si-negative control (NC) group, si-MALAT1 group, miR-129 NC group, miR-129 mimics group, p-Empty vector group, p-MALAT1 group, p-MALAT1+ miR-129 mimics group, and p-MALAT1+ si-TGIF2 group. Luciferase reporter assay, Cell Counting Kit-8 assay, Transwell assay, quantitative reverse transcription PCR, Western blot, and Pearson correlation analysis were performed. RESULTS: MALAT1 expression in tumor tissues and MG63 cells was increased (P<0.01). High MALAT1 expression predicted poor prognosis of osteosarcoma patients. MG63 cells of si-MALAT1 group exhibited much lower cell viability, migration, and invasive cell numbers when compared with si-NC group (P<0.01). For MG63 cells of miR-129 mimics group, they had markedly lower cell viability, migration, and invasive cell numbers than miR-129 NC group (P<0.01). miR-129 was targetedly and negatively regulated by MALAT1. TGIF2, which was targetedly and negatively regulated by miR-129, was overexpressed in tumor tissues and MG63 cells (P<0.01). miR-129 overexpresison and TGIF2 downregulation significantly reversed the enhanced cell viability, migration, and invasion induced by MALAT1 (P<0.01). CONCLUSION: MALAT1 promotes TGIF2 expression through negative regulation of miR-129, which further promotes the proliferation, migration, and invasion of MG63 cells.
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spelling pubmed-62876642018-12-24 MALAT1 promotes proliferation, migration, and invasion of MG63 cells by upregulation of TGIF2 via negatively regulating miR-129 Liu, Kai Zhang, Yingang Liu, Liang Yuan, Qiling Onco Targets Ther Original Research PURPOSE: This article aimed to investigate the mechanism by which MALAT1 and miR-129 affected the development of osteosarcoma. METHODS: Tumor tissues and adjacent tissues of 23 osteosarcoma patients were collected. Normal osteoblasts hFOB1.19 and osteosarcoma cells MG63 were cultured. MG63 cells were transfected and grouped: si-negative control (NC) group, si-MALAT1 group, miR-129 NC group, miR-129 mimics group, p-Empty vector group, p-MALAT1 group, p-MALAT1+ miR-129 mimics group, and p-MALAT1+ si-TGIF2 group. Luciferase reporter assay, Cell Counting Kit-8 assay, Transwell assay, quantitative reverse transcription PCR, Western blot, and Pearson correlation analysis were performed. RESULTS: MALAT1 expression in tumor tissues and MG63 cells was increased (P<0.01). High MALAT1 expression predicted poor prognosis of osteosarcoma patients. MG63 cells of si-MALAT1 group exhibited much lower cell viability, migration, and invasive cell numbers when compared with si-NC group (P<0.01). For MG63 cells of miR-129 mimics group, they had markedly lower cell viability, migration, and invasive cell numbers than miR-129 NC group (P<0.01). miR-129 was targetedly and negatively regulated by MALAT1. TGIF2, which was targetedly and negatively regulated by miR-129, was overexpressed in tumor tissues and MG63 cells (P<0.01). miR-129 overexpresison and TGIF2 downregulation significantly reversed the enhanced cell viability, migration, and invasion induced by MALAT1 (P<0.01). CONCLUSION: MALAT1 promotes TGIF2 expression through negative regulation of miR-129, which further promotes the proliferation, migration, and invasion of MG63 cells. Dove Medical Press 2018-12-04 /pmc/articles/PMC6287664/ /pubmed/30584331 http://dx.doi.org/10.2147/OTT.S182993 Text en © 2018 Liu et al. This work is published and licensed by Dove Medical Press Limited The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License (http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed.
spellingShingle Original Research
Liu, Kai
Zhang, Yingang
Liu, Liang
Yuan, Qiling
MALAT1 promotes proliferation, migration, and invasion of MG63 cells by upregulation of TGIF2 via negatively regulating miR-129
title MALAT1 promotes proliferation, migration, and invasion of MG63 cells by upregulation of TGIF2 via negatively regulating miR-129
title_full MALAT1 promotes proliferation, migration, and invasion of MG63 cells by upregulation of TGIF2 via negatively regulating miR-129
title_fullStr MALAT1 promotes proliferation, migration, and invasion of MG63 cells by upregulation of TGIF2 via negatively regulating miR-129
title_full_unstemmed MALAT1 promotes proliferation, migration, and invasion of MG63 cells by upregulation of TGIF2 via negatively regulating miR-129
title_short MALAT1 promotes proliferation, migration, and invasion of MG63 cells by upregulation of TGIF2 via negatively regulating miR-129
title_sort malat1 promotes proliferation, migration, and invasion of mg63 cells by upregulation of tgif2 via negatively regulating mir-129
topic Original Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6287664/
https://www.ncbi.nlm.nih.gov/pubmed/30584331
http://dx.doi.org/10.2147/OTT.S182993
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