Growth hormone receptor promotes osteosarcoma cell growth and metastases
Osteosarcoma (OS) is the primary bone malignancy in children and adolescents, with a high incidence of lung metastasis and poor prognosis. Here, we report that growth hormone receptor (GHR) is overexpressed in OS samples compared with osteofibrous dysplasia. We subsequently demonstrated that GHR kno...
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Online Access: | https://doi.org/10.1002/2211-5463.12761 |
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doaj-45077031e89342e8a4445cff5f7dfc762020-11-25T03:17:13ZengWileyFEBS Open Bio2211-54632020-01-0110112713410.1002/2211-5463.12761Growth hormone receptor promotes osteosarcoma cell growth and metastasesMo Cheng0Wending Huang1Weiluo Cai2Meng Fang3Yong Chen4Chunmeng Wang5Wangjun Yan6Department of Musculoskeletal Surgery Fudan University Shanghai Cancer Center ChinaDepartment of Musculoskeletal Surgery Fudan University Shanghai Cancer Center ChinaDepartment of Musculoskeletal Surgery Fudan University Shanghai Cancer Center ChinaDepartment of Musculoskeletal Surgery Fudan University Shanghai Cancer Center ChinaDepartment of Musculoskeletal Surgery Fudan University Shanghai Cancer Center ChinaDepartment of Musculoskeletal Surgery Fudan University Shanghai Cancer Center ChinaDepartment of Musculoskeletal Surgery Fudan University Shanghai Cancer Center ChinaOsteosarcoma (OS) is the primary bone malignancy in children and adolescents, with a high incidence of lung metastasis and poor prognosis. Here, we report that growth hormone receptor (GHR) is overexpressed in OS samples compared with osteofibrous dysplasia. We subsequently demonstrated that GHR knockdown inhibited colony formation, promoted cell apoptosis and decreased the number of cells at G2/M phase in 143B and U2OS cells. Furthermore, knockdown of GHR inhibited tumor growth in vivo. Together, these findings indicate that GHR modulates cell proliferation and metastasis through the phosphoinositide 3‐kinase/AKT signaling pathway and may be suitable for use as a putative biomarker of OS.https://doi.org/10.1002/2211-5463.12761growth hormone receptormetastasisosteosarcomaproliferationtumor growth |
collection |
DOAJ |
language |
English |
format |
Article |
sources |
DOAJ |
author |
Mo Cheng Wending Huang Weiluo Cai Meng Fang Yong Chen Chunmeng Wang Wangjun Yan |
spellingShingle |
Mo Cheng Wending Huang Weiluo Cai Meng Fang Yong Chen Chunmeng Wang Wangjun Yan Growth hormone receptor promotes osteosarcoma cell growth and metastases FEBS Open Bio growth hormone receptor metastasis osteosarcoma proliferation tumor growth |
author_facet |
Mo Cheng Wending Huang Weiluo Cai Meng Fang Yong Chen Chunmeng Wang Wangjun Yan |
author_sort |
Mo Cheng |
title |
Growth hormone receptor promotes osteosarcoma cell growth and metastases |
title_short |
Growth hormone receptor promotes osteosarcoma cell growth and metastases |
title_full |
Growth hormone receptor promotes osteosarcoma cell growth and metastases |
title_fullStr |
Growth hormone receptor promotes osteosarcoma cell growth and metastases |
title_full_unstemmed |
Growth hormone receptor promotes osteosarcoma cell growth and metastases |
title_sort |
growth hormone receptor promotes osteosarcoma cell growth and metastases |
publisher |
Wiley |
series |
FEBS Open Bio |
issn |
2211-5463 |
publishDate |
2020-01-01 |
description |
Osteosarcoma (OS) is the primary bone malignancy in children and adolescents, with a high incidence of lung metastasis and poor prognosis. Here, we report that growth hormone receptor (GHR) is overexpressed in OS samples compared with osteofibrous dysplasia. We subsequently demonstrated that GHR knockdown inhibited colony formation, promoted cell apoptosis and decreased the number of cells at G2/M phase in 143B and U2OS cells. Furthermore, knockdown of GHR inhibited tumor growth in vivo. Together, these findings indicate that GHR modulates cell proliferation and metastasis through the phosphoinositide 3‐kinase/AKT signaling pathway and may be suitable for use as a putative biomarker of OS. |
topic |
growth hormone receptor metastasis osteosarcoma proliferation tumor growth |
url |
https://doi.org/10.1002/2211-5463.12761 |
work_keys_str_mv |
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