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LncRNA CCAL Promotes Angiogenesis Through Regulating the MiR-29b/ANGPTL4 Axis in Osteosarcoma

PURPOSE: The objective of this study was to detect the expression of the long noncoding RNA (lncRNA) colorectal cancer-associated lncRNA (CCAL) in osteosarcoma tissues and to investigate its role in angiogenesis and the potential molecular mechanisms associated with this effect in osteosarcoma. MATE...

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Autores principales: Chen, Shiyi, Yang, Mingjia, Chang, Shimin
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Dove 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7591080/
https://www.ncbi.nlm.nih.gov/pubmed/33122950
http://dx.doi.org/10.2147/CMAR.S272230
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author Chen, Shiyi
Yang, Mingjia
Chang, Shimin
author_facet Chen, Shiyi
Yang, Mingjia
Chang, Shimin
author_sort Chen, Shiyi
collection PubMed
description PURPOSE: The objective of this study was to detect the expression of the long noncoding RNA (lncRNA) colorectal cancer-associated lncRNA (CCAL) in osteosarcoma tissues and to investigate its role in angiogenesis and the potential molecular mechanisms associated with this effect in osteosarcoma. MATERIALS AND METHODS: CCAL expression in 40 osteosarcoma tissues and 40 noncancerous tissues was measured by qRT-PCR (quantitative real-time polymerase chain reaction). Tube formation assays were performed to explore the role of CCAL in angiogenesis in osteosarcoma. In addition, the regulatory interaction between CCAL, miR-29b, and ANGPTL4 was investigated via luciferase reporter assay and bioinformatics predictive analysis. RESULTS: Compared with noncancerous tissues, the expression of CCAL was markedly upregulated in osteosarcoma tissues. Higher CCAL expression levels were closely related to shorter overall survival in patients with osteosarcoma. Additionally, functional analysis indicated that CCAL could facilitate tumour angiogenesis in vitro and in vivo in osteosarcoma. Mechanistically, CCAL upregulated ANGPTL4 expression in osteosarcoma cells, and ANGPTL4 mediated angiogenic induction by CCAL in osteosarcoma. Moreover, CCAL directly targeted miR-29b in osteosarcoma. More importantly, we demonstrated that CCAL upregulated the expression of ANGPTL4 by sponging miR-29b, which promoted angiogenesis in osteosarcoma. CONCLUSION: Our results show that CCAL promotes angiogenesis by regulating the miR-29b/ANGPTL4 axis in osteosarcoma.
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spelling pubmed-75910802020-10-28 LncRNA CCAL Promotes Angiogenesis Through Regulating the MiR-29b/ANGPTL4 Axis in Osteosarcoma Chen, Shiyi Yang, Mingjia Chang, Shimin Cancer Manag Res Original Research PURPOSE: The objective of this study was to detect the expression of the long noncoding RNA (lncRNA) colorectal cancer-associated lncRNA (CCAL) in osteosarcoma tissues and to investigate its role in angiogenesis and the potential molecular mechanisms associated with this effect in osteosarcoma. MATERIALS AND METHODS: CCAL expression in 40 osteosarcoma tissues and 40 noncancerous tissues was measured by qRT-PCR (quantitative real-time polymerase chain reaction). Tube formation assays were performed to explore the role of CCAL in angiogenesis in osteosarcoma. In addition, the regulatory interaction between CCAL, miR-29b, and ANGPTL4 was investigated via luciferase reporter assay and bioinformatics predictive analysis. RESULTS: Compared with noncancerous tissues, the expression of CCAL was markedly upregulated in osteosarcoma tissues. Higher CCAL expression levels were closely related to shorter overall survival in patients with osteosarcoma. Additionally, functional analysis indicated that CCAL could facilitate tumour angiogenesis in vitro and in vivo in osteosarcoma. Mechanistically, CCAL upregulated ANGPTL4 expression in osteosarcoma cells, and ANGPTL4 mediated angiogenic induction by CCAL in osteosarcoma. Moreover, CCAL directly targeted miR-29b in osteosarcoma. More importantly, we demonstrated that CCAL upregulated the expression of ANGPTL4 by sponging miR-29b, which promoted angiogenesis in osteosarcoma. CONCLUSION: Our results show that CCAL promotes angiogenesis by regulating the miR-29b/ANGPTL4 axis in osteosarcoma. Dove 2020-10-23 /pmc/articles/PMC7591080/ /pubmed/33122950 http://dx.doi.org/10.2147/CMAR.S272230 Text en © 2020 Chen et al. http://creativecommons.org/licenses/by-nc/3.0/ 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. For permission for commercial use of this work, please see paragraphs 4.2 and 5 of our Terms (https://www.dovepress.com/terms.php).
spellingShingle Original Research
Chen, Shiyi
Yang, Mingjia
Chang, Shimin
LncRNA CCAL Promotes Angiogenesis Through Regulating the MiR-29b/ANGPTL4 Axis in Osteosarcoma
title LncRNA CCAL Promotes Angiogenesis Through Regulating the MiR-29b/ANGPTL4 Axis in Osteosarcoma
title_full LncRNA CCAL Promotes Angiogenesis Through Regulating the MiR-29b/ANGPTL4 Axis in Osteosarcoma
title_fullStr LncRNA CCAL Promotes Angiogenesis Through Regulating the MiR-29b/ANGPTL4 Axis in Osteosarcoma
title_full_unstemmed LncRNA CCAL Promotes Angiogenesis Through Regulating the MiR-29b/ANGPTL4 Axis in Osteosarcoma
title_short LncRNA CCAL Promotes Angiogenesis Through Regulating the MiR-29b/ANGPTL4 Axis in Osteosarcoma
title_sort lncrna ccal promotes angiogenesis through regulating the mir-29b/angptl4 axis in osteosarcoma
topic Original Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7591080/
https://www.ncbi.nlm.nih.gov/pubmed/33122950
http://dx.doi.org/10.2147/CMAR.S272230
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AT changshimin lncrnaccalpromotesangiogenesisthroughregulatingthemir29bangptl4axisinosteosarcoma