Long non-coding HOXA-AS3 contributes to osteosarcoma progression through the miR-1286/TEAD1 axis

Long non-coding RNA (lncRNA) HOXA cluster antisense RNA 3 (HOXA-AS3) regulates the progression of several types of human malignancy. However, the role and potential mechanism of HOXA-AS3 in osteosarcoma (OS) remain unknown. In this study, upregulation of HOXA-AS3 was observed in OS tissues and cell...

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Autores principales: Xiao, Xiangjun, Liu, Mingjiang, Xie, Songlin, Liu, Changxiong, Huang, Xinfeng, Huang, Xiongjie
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2023
Materias:
Research Article
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10523635/
https://www.ncbi.nlm.nih.gov/pubmed/37752588
http://dx.doi.org/10.1186/s13018-023-04214-5
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author Xiao, Xiangjun
Liu, Mingjiang
Xie, Songlin
Liu, Changxiong
Huang, Xinfeng
Huang, Xiongjie
author_facet Xiao, Xiangjun
Liu, Mingjiang
Xie, Songlin
Liu, Changxiong
Huang, Xinfeng
Huang, Xiongjie
author_sort Xiao, Xiangjun
collection PubMed
description Long non-coding RNA (lncRNA) HOXA cluster antisense RNA 3 (HOXA-AS3) regulates the progression of several types of human malignancy. However, the role and potential mechanism of HOXA-AS3 in osteosarcoma (OS) remain unknown. In this study, upregulation of HOXA-AS3 was observed in OS tissues and cell lines and associated with poor clinical outcomes. Silencing of HOXA-AS3 significantly inhibited the proliferation, migration and invasion of OS cells in vitro and suppressed the tumorigenesis of OS cells in vivo. Furthermore, knockdown of HOXA-AS3 inhibited the proliferation and migration of human umbilical vein endothelial cells (HUVECs) and epithelial-to-mesenchymal transition (EMT) in OS. Further investigation of this mechanism revealed that HOXA-AS3 could directly upregulate the expression of TEAD1 via its competing endogenous RNA (ceRNA) activity on miR-1286. This study clarified the oncogenic roles of the HOXA-AS3/miR-1286/TEAD1 axis in OS progression, suggesting a novel therapeutic target for OS. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1186/s13018-023-04214-5.
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spelling pubmed-105236352023-09-28 Long non-coding HOXA-AS3 contributes to osteosarcoma progression through the miR-1286/TEAD1 axis Xiao, Xiangjun Liu, Mingjiang Xie, Songlin Liu, Changxiong Huang, Xinfeng Huang, Xiongjie J Orthop Surg Res Research Article Long non-coding RNA (lncRNA) HOXA cluster antisense RNA 3 (HOXA-AS3) regulates the progression of several types of human malignancy. However, the role and potential mechanism of HOXA-AS3 in osteosarcoma (OS) remain unknown. In this study, upregulation of HOXA-AS3 was observed in OS tissues and cell lines and associated with poor clinical outcomes. Silencing of HOXA-AS3 significantly inhibited the proliferation, migration and invasion of OS cells in vitro and suppressed the tumorigenesis of OS cells in vivo. Furthermore, knockdown of HOXA-AS3 inhibited the proliferation and migration of human umbilical vein endothelial cells (HUVECs) and epithelial-to-mesenchymal transition (EMT) in OS. Further investigation of this mechanism revealed that HOXA-AS3 could directly upregulate the expression of TEAD1 via its competing endogenous RNA (ceRNA) activity on miR-1286. This study clarified the oncogenic roles of the HOXA-AS3/miR-1286/TEAD1 axis in OS progression, suggesting a novel therapeutic target for OS. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1186/s13018-023-04214-5. BioMed Central 2023-09-27 /pmc/articles/PMC10523635/ /pubmed/37752588 http://dx.doi.org/10.1186/s13018-023-04214-5 Text en © The Author(s) 2023 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 licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence 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 licence, visit http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) . The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/ (https://creativecommons.org/publicdomain/zero/1.0/) ) applies to the data made available in this article, unless otherwise stated in a credit line to the data.
spellingShingle Research Article
Xiao, Xiangjun
Liu, Mingjiang
Xie, Songlin
Liu, Changxiong
Huang, Xinfeng
Huang, Xiongjie
Long non-coding HOXA-AS3 contributes to osteosarcoma progression through the miR-1286/TEAD1 axis
title Long non-coding HOXA-AS3 contributes to osteosarcoma progression through the miR-1286/TEAD1 axis
title_full Long non-coding HOXA-AS3 contributes to osteosarcoma progression through the miR-1286/TEAD1 axis
title_fullStr Long non-coding HOXA-AS3 contributes to osteosarcoma progression through the miR-1286/TEAD1 axis
title_full_unstemmed Long non-coding HOXA-AS3 contributes to osteosarcoma progression through the miR-1286/TEAD1 axis
title_short Long non-coding HOXA-AS3 contributes to osteosarcoma progression through the miR-1286/TEAD1 axis
title_sort long non-coding hoxa-as3 contributes to osteosarcoma progression through the mir-1286/tead1 axis
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10523635/
https://www.ncbi.nlm.nih.gov/pubmed/37752588
http://dx.doi.org/10.1186/s13018-023-04214-5
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