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SPC24 promotes osteosarcoma progression by increasing EGFR/MAPK signaling

In this study, we investigated the role of the spindle checkpoint protein SPC24 in osteosarcoma progression. SPC24 knockdown in 143B and U2OS osteosarcoma cells decreased cell growth, survival and invasiveness. The SPC24 knockdown cells also exhibited low EGFR, Ras and phospho-ERK levels and high E-...

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Autores principales: Sheng, Jun, Yin, Mengchen, Sun, Zhengwang, Kang, Xia, Liu, Da, Jiang, Kai, Xu, Jia, Zhao, Feixing, Guo, Qunfeng, Zheng, Wei
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Impact Journals LLC 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5739637/
https://www.ncbi.nlm.nih.gov/pubmed/29285250
http://dx.doi.org/10.18632/oncotarget.22167
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author Sheng, Jun
Yin, Mengchen
Sun, Zhengwang
Kang, Xia
Liu, Da
Jiang, Kai
Xu, Jia
Zhao, Feixing
Guo, Qunfeng
Zheng, Wei
author_facet Sheng, Jun
Yin, Mengchen
Sun, Zhengwang
Kang, Xia
Liu, Da
Jiang, Kai
Xu, Jia
Zhao, Feixing
Guo, Qunfeng
Zheng, Wei
author_sort Sheng, Jun
collection PubMed
description In this study, we investigated the role of the spindle checkpoint protein SPC24 in osteosarcoma progression. SPC24 knockdown in 143B and U2OS osteosarcoma cells decreased cell growth, survival and invasiveness. The SPC24 knockdown cells also exhibited low EGFR, Ras and phospho-ERK levels and high E-cadherin levels, suggesting inhibition of EGFR/Ras/ERK signaling and epithelial-to-mesenchymal transitioning. Xenografted SPC24 knockdown osteosarcoma cells showed reduced tumor growth in nude mice with decreased EGFR and phospho-ERK levels and increased E-cadherin levels. By contrast, human osteosarcoma tissue samples showed high SPC24 and phospho-ERK levels and low E-cadherin levels. These results suggest SPC24 promotes osteosarcoma progression by increasing EGFR/Ras/ERK signaling.
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spelling pubmed-57396372017-12-28 SPC24 promotes osteosarcoma progression by increasing EGFR/MAPK signaling Sheng, Jun Yin, Mengchen Sun, Zhengwang Kang, Xia Liu, Da Jiang, Kai Xu, Jia Zhao, Feixing Guo, Qunfeng Zheng, Wei Oncotarget Research Paper In this study, we investigated the role of the spindle checkpoint protein SPC24 in osteosarcoma progression. SPC24 knockdown in 143B and U2OS osteosarcoma cells decreased cell growth, survival and invasiveness. The SPC24 knockdown cells also exhibited low EGFR, Ras and phospho-ERK levels and high E-cadherin levels, suggesting inhibition of EGFR/Ras/ERK signaling and epithelial-to-mesenchymal transitioning. Xenografted SPC24 knockdown osteosarcoma cells showed reduced tumor growth in nude mice with decreased EGFR and phospho-ERK levels and increased E-cadherin levels. By contrast, human osteosarcoma tissue samples showed high SPC24 and phospho-ERK levels and low E-cadherin levels. These results suggest SPC24 promotes osteosarcoma progression by increasing EGFR/Ras/ERK signaling. Impact Journals LLC 2017-10-27 /pmc/articles/PMC5739637/ /pubmed/29285250 http://dx.doi.org/10.18632/oncotarget.22167 Text en Copyright: © 2017 Sheng et al. http://creativecommons.org/licenses/by/3.0/ This article is distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0/) (CC-BY), which permits unrestricted use and redistribution provided that the original author and source are credited.
spellingShingle Research Paper
Sheng, Jun
Yin, Mengchen
Sun, Zhengwang
Kang, Xia
Liu, Da
Jiang, Kai
Xu, Jia
Zhao, Feixing
Guo, Qunfeng
Zheng, Wei
SPC24 promotes osteosarcoma progression by increasing EGFR/MAPK signaling
title SPC24 promotes osteosarcoma progression by increasing EGFR/MAPK signaling
title_full SPC24 promotes osteosarcoma progression by increasing EGFR/MAPK signaling
title_fullStr SPC24 promotes osteosarcoma progression by increasing EGFR/MAPK signaling
title_full_unstemmed SPC24 promotes osteosarcoma progression by increasing EGFR/MAPK signaling
title_short SPC24 promotes osteosarcoma progression by increasing EGFR/MAPK signaling
title_sort spc24 promotes osteosarcoma progression by increasing egfr/mapk signaling
topic Research Paper
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5739637/
https://www.ncbi.nlm.nih.gov/pubmed/29285250
http://dx.doi.org/10.18632/oncotarget.22167
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