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CEACAM6 is associated with osteosarcoma metastasis and facilitates epithelial–mesenchymal transition in osteosarcoma cells

BACKGROUND: Carcinoembryonic antigen-related cell adhesion molecule 6 (CEACAM6) is a member of CEACAM family and has been reported to be upregulated in various types of human cancer and involved in tumor progression and metastasis. However, the biological roles and clinical significances of CEACAM6...

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Detalles Bibliográficos
Autores principales: Wang, Zeyu, Luo, Chong, Wang, Huidan, Yan, Xia, Liu, Wei, Meng, Zengdong
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Dove Medical Press 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5983009/
https://www.ncbi.nlm.nih.gov/pubmed/29881289
http://dx.doi.org/10.2147/OTT.S161807
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author Wang, Zeyu
Luo, Chong
Wang, Huidan
Yan, Xia
Liu, Wei
Meng, Zengdong
author_facet Wang, Zeyu
Luo, Chong
Wang, Huidan
Yan, Xia
Liu, Wei
Meng, Zengdong
author_sort Wang, Zeyu
collection PubMed
description BACKGROUND: Carcinoembryonic antigen-related cell adhesion molecule 6 (CEACAM6) is a member of CEACAM family and has been reported to be upregulated in various types of human cancer and involved in tumor progression and metastasis. However, the biological roles and clinical significances of CEACAM6 in osteosarcoma still remain to be elucidated. MATERIALS AND METHODS: Real-timePCR, immunohistochemistry and Western blot analysis were used to determine CEACAM6 expression in osteosarcoma cell lines and clinical specimens. Then the clinical relevance of CEACAM6 was analyzed in osteosarcoma. The function of CEACAM6 in osteosarcoma was examined by wound-healing and cell invasion assays, and expression levels of epithelial–mesenchymal transition markers. RESULTS: In the present study, we found that CEACAM6 was markedly upregulated in metastatic osteosarcoma tissues when compared with the nonmetastatic osteosarcoma tissues. Upregulation of CEACAM6 was significantly associated with lung metastasis status (P=0.006) in patients with osteosarcoma. Survival analyses suggested that osteosarcoma patients with high CEACAM6 expression had a significantly shorter overall survival time and lung metastasis-free survival time than those with low CEACAM6 expression. Knockdown of CEACAM6 inhibits osteosarcoma cell migration and invasion. Moreover, silencing CEACAM6 suppressed osteosarcoma cells epithelial–mesenchymal transition. CONCLUSION: Taken together, this study suggests that CEACAM6 might be a promising biomarker and a potential therapeutic target for the treatment of metastatic osteosarcoma.
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spelling pubmed-59830092018-06-07 CEACAM6 is associated with osteosarcoma metastasis and facilitates epithelial–mesenchymal transition in osteosarcoma cells Wang, Zeyu Luo, Chong Wang, Huidan Yan, Xia Liu, Wei Meng, Zengdong Onco Targets Ther Original Research BACKGROUND: Carcinoembryonic antigen-related cell adhesion molecule 6 (CEACAM6) is a member of CEACAM family and has been reported to be upregulated in various types of human cancer and involved in tumor progression and metastasis. However, the biological roles and clinical significances of CEACAM6 in osteosarcoma still remain to be elucidated. MATERIALS AND METHODS: Real-timePCR, immunohistochemistry and Western blot analysis were used to determine CEACAM6 expression in osteosarcoma cell lines and clinical specimens. Then the clinical relevance of CEACAM6 was analyzed in osteosarcoma. The function of CEACAM6 in osteosarcoma was examined by wound-healing and cell invasion assays, and expression levels of epithelial–mesenchymal transition markers. RESULTS: In the present study, we found that CEACAM6 was markedly upregulated in metastatic osteosarcoma tissues when compared with the nonmetastatic osteosarcoma tissues. Upregulation of CEACAM6 was significantly associated with lung metastasis status (P=0.006) in patients with osteosarcoma. Survival analyses suggested that osteosarcoma patients with high CEACAM6 expression had a significantly shorter overall survival time and lung metastasis-free survival time than those with low CEACAM6 expression. Knockdown of CEACAM6 inhibits osteosarcoma cell migration and invasion. Moreover, silencing CEACAM6 suppressed osteosarcoma cells epithelial–mesenchymal transition. CONCLUSION: Taken together, this study suggests that CEACAM6 might be a promising biomarker and a potential therapeutic target for the treatment of metastatic osteosarcoma. Dove Medical Press 2018-05-28 /pmc/articles/PMC5983009/ /pubmed/29881289 http://dx.doi.org/10.2147/OTT.S161807 Text en © 2018 Wang et al. 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.
spellingShingle Original Research
Wang, Zeyu
Luo, Chong
Wang, Huidan
Yan, Xia
Liu, Wei
Meng, Zengdong
CEACAM6 is associated with osteosarcoma metastasis and facilitates epithelial–mesenchymal transition in osteosarcoma cells
title CEACAM6 is associated with osteosarcoma metastasis and facilitates epithelial–mesenchymal transition in osteosarcoma cells
title_full CEACAM6 is associated with osteosarcoma metastasis and facilitates epithelial–mesenchymal transition in osteosarcoma cells
title_fullStr CEACAM6 is associated with osteosarcoma metastasis and facilitates epithelial–mesenchymal transition in osteosarcoma cells
title_full_unstemmed CEACAM6 is associated with osteosarcoma metastasis and facilitates epithelial–mesenchymal transition in osteosarcoma cells
title_short CEACAM6 is associated with osteosarcoma metastasis and facilitates epithelial–mesenchymal transition in osteosarcoma cells
title_sort ceacam6 is associated with osteosarcoma metastasis and facilitates epithelial–mesenchymal transition in osteosarcoma cells
topic Original Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5983009/
https://www.ncbi.nlm.nih.gov/pubmed/29881289
http://dx.doi.org/10.2147/OTT.S161807
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