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von Willebrand factor rescued by miR-24 inhibition facilitates the proliferation and migration of osteosarcoma cells in vitro

von Willebrand factor (vWF) is a major procoagulant molecule that was shown to differentiate between metastatic and primary osteosarcoma (OS) tissues and associated with increased metastasis. However, its functional role in OS progression has been unclear yet. The expression profile of vWF and miR-2...

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Autores principales: Liu, Ling, Pan, Jun, Wang, Huan, Ma, Zhenni, Yin, Jie, Yuan, Feng, Yuan, Quanwen, Zhou, Lu, Liu, Xiaofeng, Zhang, Yu, Bao, Zhaohua, Yang, Huilin, Ling, Jing
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Portland Press Ltd. 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6240719/
https://www.ncbi.nlm.nih.gov/pubmed/30279208
http://dx.doi.org/10.1042/BSR20180372
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author Liu, Ling
Pan, Jun
Wang, Huan
Ma, Zhenni
Yin, Jie
Yuan, Feng
Yuan, Quanwen
Zhou, Lu
Liu, Xiaofeng
Zhang, Yu
Bao, Zhaohua
Yang, Huilin
Ling, Jing
author_facet Liu, Ling
Pan, Jun
Wang, Huan
Ma, Zhenni
Yin, Jie
Yuan, Feng
Yuan, Quanwen
Zhou, Lu
Liu, Xiaofeng
Zhang, Yu
Bao, Zhaohua
Yang, Huilin
Ling, Jing
author_sort Liu, Ling
collection PubMed
description von Willebrand factor (vWF) is a major procoagulant molecule that was shown to differentiate between metastatic and primary osteosarcoma (OS) tissues and associated with increased metastasis. However, its functional role in OS progression has been unclear yet. The expression profile of vWF and miR-24 in human OS tissues was characterized using immunofluorescence labeling and quantitative real-time PCR analysis. The interaction between miR-24 and vWF was identified by dual luciferase reporter assay. The effects of vWF and miR-24 on OS cells were assessed by cell proliferation, colony formation, and migration. The clinical significance of miR-24 in OS patients was analyzed using Kaplan–Meier analyses and Pearson’s Chi-squared test. Here, we reported that the expression of vWF was significantly increased, but miR-24 was significantly decreased in OS tissues (n=84). vWF was further validated as the target of miR-24 in MG-63 and U2OS cells. miR-24 obviously suppressed the proliferation and migration of MG-63 and U2OS cells. However, the migration-inhibiting activity of miR-24 was predominantly attenuated by vWF overexpression. Clinically, low miR-24 expression in human OS tissues was significantly associated with tumor metastasis and predicted a poor survival in OS patients. This work demonstrated that vWF, as a downstream effector of miR-24, played an important role in controlling OS cell progression. Target miR-24 or vWF, therefore, promises to be an effective biological target for OS treatment.
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spelling pubmed-62407192018-11-28 von Willebrand factor rescued by miR-24 inhibition facilitates the proliferation and migration of osteosarcoma cells in vitro Liu, Ling Pan, Jun Wang, Huan Ma, Zhenni Yin, Jie Yuan, Feng Yuan, Quanwen Zhou, Lu Liu, Xiaofeng Zhang, Yu Bao, Zhaohua Yang, Huilin Ling, Jing Biosci Rep Research Articles von Willebrand factor (vWF) is a major procoagulant molecule that was shown to differentiate between metastatic and primary osteosarcoma (OS) tissues and associated with increased metastasis. However, its functional role in OS progression has been unclear yet. The expression profile of vWF and miR-24 in human OS tissues was characterized using immunofluorescence labeling and quantitative real-time PCR analysis. The interaction between miR-24 and vWF was identified by dual luciferase reporter assay. The effects of vWF and miR-24 on OS cells were assessed by cell proliferation, colony formation, and migration. The clinical significance of miR-24 in OS patients was analyzed using Kaplan–Meier analyses and Pearson’s Chi-squared test. Here, we reported that the expression of vWF was significantly increased, but miR-24 was significantly decreased in OS tissues (n=84). vWF was further validated as the target of miR-24 in MG-63 and U2OS cells. miR-24 obviously suppressed the proliferation and migration of MG-63 and U2OS cells. However, the migration-inhibiting activity of miR-24 was predominantly attenuated by vWF overexpression. Clinically, low miR-24 expression in human OS tissues was significantly associated with tumor metastasis and predicted a poor survival in OS patients. This work demonstrated that vWF, as a downstream effector of miR-24, played an important role in controlling OS cell progression. Target miR-24 or vWF, therefore, promises to be an effective biological target for OS treatment. Portland Press Ltd. 2018-11-16 /pmc/articles/PMC6240719/ /pubmed/30279208 http://dx.doi.org/10.1042/BSR20180372 Text en © 2018 The Author(s). http://creativecommons.org/licenses/by/4.0/This is an open access article published by Portland Press Limited on behalf of the Biochemical Society and distributed under the Creative Commons Attribution License 4.0 (CC BY) (http://creativecommons.org/licenses/by/4.0/) .
spellingShingle Research Articles
Liu, Ling
Pan, Jun
Wang, Huan
Ma, Zhenni
Yin, Jie
Yuan, Feng
Yuan, Quanwen
Zhou, Lu
Liu, Xiaofeng
Zhang, Yu
Bao, Zhaohua
Yang, Huilin
Ling, Jing
von Willebrand factor rescued by miR-24 inhibition facilitates the proliferation and migration of osteosarcoma cells in vitro
title von Willebrand factor rescued by miR-24 inhibition facilitates the proliferation and migration of osteosarcoma cells in vitro
title_full von Willebrand factor rescued by miR-24 inhibition facilitates the proliferation and migration of osteosarcoma cells in vitro
title_fullStr von Willebrand factor rescued by miR-24 inhibition facilitates the proliferation and migration of osteosarcoma cells in vitro
title_full_unstemmed von Willebrand factor rescued by miR-24 inhibition facilitates the proliferation and migration of osteosarcoma cells in vitro
title_short von Willebrand factor rescued by miR-24 inhibition facilitates the proliferation and migration of osteosarcoma cells in vitro
title_sort von willebrand factor rescued by mir-24 inhibition facilitates the proliferation and migration of osteosarcoma cells in vitro
topic Research Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6240719/
https://www.ncbi.nlm.nih.gov/pubmed/30279208
http://dx.doi.org/10.1042/BSR20180372
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