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lncRNA MALAT1 regulated ATAD2 to facilitate retinoblastoma progression via miR-655-3p

Long noncoding RNA (lncRNA) metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) was reported as an oncogene in many tumors including retinoblastoma (RB). This research mainly focused on the functions and mechanism of MALAT1 in RB. MALAT1 was upregulated in RB tissues and cells, and it se...

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Autores principales: Zhao, Yuxin, Wang, Zhaoxia, Gao, Meili, Wang, Xuehong, Feng, Hui, Cui, Yuanyuan, Tian, Xia
Formato: Online Artículo Texto
Lenguaje:English
Publicado: De Gruyter 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8231467/
https://www.ncbi.nlm.nih.gov/pubmed/34222668
http://dx.doi.org/10.1515/med-2021-0290
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author Zhao, Yuxin
Wang, Zhaoxia
Gao, Meili
Wang, Xuehong
Feng, Hui
Cui, Yuanyuan
Tian, Xia
author_facet Zhao, Yuxin
Wang, Zhaoxia
Gao, Meili
Wang, Xuehong
Feng, Hui
Cui, Yuanyuan
Tian, Xia
author_sort Zhao, Yuxin
collection PubMed
description Long noncoding RNA (lncRNA) metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) was reported as an oncogene in many tumors including retinoblastoma (RB). This research mainly focused on the functions and mechanism of MALAT1 in RB. MALAT1 was upregulated in RB tissues and cells, and it served as a competing endogenous RNA (ceRNA) and inhibited miRNA-655-3p (miR-655-3p) expression, which eventually regulated the expression of miR-655-3p downstream target ATPase Family AAA Domain Containing 2 (ATAD2). The level of ATAD2 significantly increased, while that of miR-655-3p remarkably decreased in RB tissues and cells. MALAT1 depletion inhibited cell proliferation, metastasis, and epithelial–mesenchymal transition (EMT), but promoted apoptosis in vitro and blocked xenograft tumor growth in vivo. MALAT1 exerted its oncogenic functions in RB by regulating miR-655-3p/ATAD2 axis.
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spelling pubmed-82314672021-07-01 lncRNA MALAT1 regulated ATAD2 to facilitate retinoblastoma progression via miR-655-3p Zhao, Yuxin Wang, Zhaoxia Gao, Meili Wang, Xuehong Feng, Hui Cui, Yuanyuan Tian, Xia Open Med (Wars) Research Article Long noncoding RNA (lncRNA) metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) was reported as an oncogene in many tumors including retinoblastoma (RB). This research mainly focused on the functions and mechanism of MALAT1 in RB. MALAT1 was upregulated in RB tissues and cells, and it served as a competing endogenous RNA (ceRNA) and inhibited miRNA-655-3p (miR-655-3p) expression, which eventually regulated the expression of miR-655-3p downstream target ATPase Family AAA Domain Containing 2 (ATAD2). The level of ATAD2 significantly increased, while that of miR-655-3p remarkably decreased in RB tissues and cells. MALAT1 depletion inhibited cell proliferation, metastasis, and epithelial–mesenchymal transition (EMT), but promoted apoptosis in vitro and blocked xenograft tumor growth in vivo. MALAT1 exerted its oncogenic functions in RB by regulating miR-655-3p/ATAD2 axis. De Gruyter 2021-06-24 /pmc/articles/PMC8231467/ /pubmed/34222668 http://dx.doi.org/10.1515/med-2021-0290 Text en © 2021 Yuxin Zhao et al., published by De Gruyter https://creativecommons.org/licenses/by/4.0/This work is licensed under the Creative Commons Attribution 4.0 International License.
spellingShingle Research Article
Zhao, Yuxin
Wang, Zhaoxia
Gao, Meili
Wang, Xuehong
Feng, Hui
Cui, Yuanyuan
Tian, Xia
lncRNA MALAT1 regulated ATAD2 to facilitate retinoblastoma progression via miR-655-3p
title lncRNA MALAT1 regulated ATAD2 to facilitate retinoblastoma progression via miR-655-3p
title_full lncRNA MALAT1 regulated ATAD2 to facilitate retinoblastoma progression via miR-655-3p
title_fullStr lncRNA MALAT1 regulated ATAD2 to facilitate retinoblastoma progression via miR-655-3p
title_full_unstemmed lncRNA MALAT1 regulated ATAD2 to facilitate retinoblastoma progression via miR-655-3p
title_short lncRNA MALAT1 regulated ATAD2 to facilitate retinoblastoma progression via miR-655-3p
title_sort lncrna malat1 regulated atad2 to facilitate retinoblastoma progression via mir-655-3p
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8231467/
https://www.ncbi.nlm.nih.gov/pubmed/34222668
http://dx.doi.org/10.1515/med-2021-0290
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