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Cancer stem cell marker CD90 inhibits ovarian cancer formation via β3 integrin
Cancer stem cell (CSC) markers have been identified for CSC isolation and proposed as therapeutic targets in various types of cancers. CD90, one of the characterized markers in liver and gastric cancer, is shown to promote cancer formation. However, the underexpression level of CD90 in ovarian cance...
Autores principales: | , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
D.A. Spandidos
2016
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5063452/ https://www.ncbi.nlm.nih.gov/pubmed/27633757 http://dx.doi.org/10.3892/ijo.2016.3691 |
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author | Chen, Wei-Ching Hsu, Hui-Ping Li, Chung-Yen Yang, Ya-Ju Hung, Yu-Hsuan Cho, Chien-Yu Wang, Chih-Yang Weng, Tzu-Yang Lai, Ming-Derg |
author_facet | Chen, Wei-Ching Hsu, Hui-Ping Li, Chung-Yen Yang, Ya-Ju Hung, Yu-Hsuan Cho, Chien-Yu Wang, Chih-Yang Weng, Tzu-Yang Lai, Ming-Derg |
author_sort | Chen, Wei-Ching |
collection | PubMed |
description | Cancer stem cell (CSC) markers have been identified for CSC isolation and proposed as therapeutic targets in various types of cancers. CD90, one of the characterized markers in liver and gastric cancer, is shown to promote cancer formation. However, the underexpression level of CD90 in ovarian cancer cells and the evidence supporting the cellular mechanism have not been investigated. In the present study, we found that the DNA copy number of CD90 is correlated with mRNA expression in ovarian cancer tissue and the ovarian cancer patients with higher CD90 have good prognosis compared to the patients with lower CD90. Although the expression of CD90 in human ovarian cancer SKOV3 cells enhances the cell proliferation by MTT and anchorage-dependent growth assay, CD90 inhibits the anchorage-independent growth ability in vitro and tumor formation in vivo. CD90 overexpression suppresses the sphere-forming ability and ALDH activity and enhances the cell apoptosis, indicating that CD90 may reduce the cell growth by the properties of CSC and anoikis. Furthermore, CD90 reduces the expression of other CSC markers, including CD133 and CD24. The inhibition of CD133 is attenuated by the mutant CD90, which is replaced with RLE domain into RLD domain. Importantly, the CD90-regulated inhibition of CD133 expression, anchorage-independent growth and signal transduction of mTOR and AMPK are restored by the β3 integrin shRNA. Our results provide evidence that CD90 mediates the antitumor formation by interacting with β3 integrin, which provides new insight that can potentially be applied in the development of therapeutic strategies in ovarian cancer. |
format | Online Article Text |
id | pubmed-5063452 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2016 |
publisher | D.A. Spandidos |
record_format | MEDLINE/PubMed |
spelling | pubmed-50634522016-10-17 Cancer stem cell marker CD90 inhibits ovarian cancer formation via β3 integrin Chen, Wei-Ching Hsu, Hui-Ping Li, Chung-Yen Yang, Ya-Ju Hung, Yu-Hsuan Cho, Chien-Yu Wang, Chih-Yang Weng, Tzu-Yang Lai, Ming-Derg Int J Oncol Articles Cancer stem cell (CSC) markers have been identified for CSC isolation and proposed as therapeutic targets in various types of cancers. CD90, one of the characterized markers in liver and gastric cancer, is shown to promote cancer formation. However, the underexpression level of CD90 in ovarian cancer cells and the evidence supporting the cellular mechanism have not been investigated. In the present study, we found that the DNA copy number of CD90 is correlated with mRNA expression in ovarian cancer tissue and the ovarian cancer patients with higher CD90 have good prognosis compared to the patients with lower CD90. Although the expression of CD90 in human ovarian cancer SKOV3 cells enhances the cell proliferation by MTT and anchorage-dependent growth assay, CD90 inhibits the anchorage-independent growth ability in vitro and tumor formation in vivo. CD90 overexpression suppresses the sphere-forming ability and ALDH activity and enhances the cell apoptosis, indicating that CD90 may reduce the cell growth by the properties of CSC and anoikis. Furthermore, CD90 reduces the expression of other CSC markers, including CD133 and CD24. The inhibition of CD133 is attenuated by the mutant CD90, which is replaced with RLE domain into RLD domain. Importantly, the CD90-regulated inhibition of CD133 expression, anchorage-independent growth and signal transduction of mTOR and AMPK are restored by the β3 integrin shRNA. Our results provide evidence that CD90 mediates the antitumor formation by interacting with β3 integrin, which provides new insight that can potentially be applied in the development of therapeutic strategies in ovarian cancer. D.A. Spandidos 2016-09-15 /pmc/articles/PMC5063452/ /pubmed/27633757 http://dx.doi.org/10.3892/ijo.2016.3691 Text en Copyright: © Chen et al. This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License (https://creativecommons.org/licenses/by-nc-nd/4.0/) , which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made. |
spellingShingle | Articles Chen, Wei-Ching Hsu, Hui-Ping Li, Chung-Yen Yang, Ya-Ju Hung, Yu-Hsuan Cho, Chien-Yu Wang, Chih-Yang Weng, Tzu-Yang Lai, Ming-Derg Cancer stem cell marker CD90 inhibits ovarian cancer formation via β3 integrin |
title | Cancer stem cell marker CD90 inhibits ovarian cancer formation via β3 integrin |
title_full | Cancer stem cell marker CD90 inhibits ovarian cancer formation via β3 integrin |
title_fullStr | Cancer stem cell marker CD90 inhibits ovarian cancer formation via β3 integrin |
title_full_unstemmed | Cancer stem cell marker CD90 inhibits ovarian cancer formation via β3 integrin |
title_short | Cancer stem cell marker CD90 inhibits ovarian cancer formation via β3 integrin |
title_sort | cancer stem cell marker cd90 inhibits ovarian cancer formation via β3 integrin |
topic | Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5063452/ https://www.ncbi.nlm.nih.gov/pubmed/27633757 http://dx.doi.org/10.3892/ijo.2016.3691 |
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