Role of cytoplasmic localization of maspin in promoting cell invasion in breast cancer with aggressive phenotype

Abstract Mammary serine protease inhibitor (maspin) is a tumor suppressor gene that is downregulated during carcinogenesis and breast cancer progression. While the nuclear localization of maspin is essential for tumor suppression, we previously reported that the cytoplasmic localization of maspin wa...

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Autores principales:	Tomohiko Sakabe, Makoto Wakahara, Goshi Shiota, Yoshihisa Umekita
Formato:	article
Lenguaje:	EN
Publicado:	Nature Portfolio 2021
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/66d6afc5b65f4960b3332db74bc0a913
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spelling	oai:doaj.org-article:66d6afc5b65f4960b3332db74bc0a9132021-12-02T15:56:57ZRole of cytoplasmic localization of maspin in promoting cell invasion in breast cancer with aggressive phenotype10.1038/s41598-021-90887-z2045-2322https://doaj.org/article/66d6afc5b65f4960b3332db74bc0a9132021-05-01T00:00:00Zhttps://doi.org/10.1038/s41598-021-90887-zhttps://doaj.org/toc/2045-2322Abstract Mammary serine protease inhibitor (maspin) is a tumor suppressor gene that is downregulated during carcinogenesis and breast cancer progression. While the nuclear localization of maspin is essential for tumor suppression, we previously reported that the cytoplasmic localization of maspin was significantly correlated with poor prognosis in breast cancer patients. To understand the mechanisms that underlie oncogenic role of cytoplasmic maspin, we studied its biological function in breast cancer cell lines. Subcellular localization of maspin in MDA-MB-231 breast cancer cells was mainly detected in the cytoplasm, whereas in MCF10A mammary epithelial cells, maspin was present in both cytoplasm and nucleus. In MDA-MB-231 cells, maspin overexpression promoted cell proliferation and cell invasion, whereas maspin downregulation resulted in the opposite effect. Further, we observed that SRGN protein levels were increased in MDA-MB-231 cells stably overexpressing maspin. Finally, maspin overexpression in MDA-MB-231 cells resulted in the N-cadherin and epithelial mesenchymal transition (EMT)-related transcription factors upregulation, and TGFβ signaling pathway activation. These results suggested that cytoplasmic maspin enhances the invasive and metastatic potential in breast cancer cells with aggressive phenotype by inducing EMT via SRGN/TGFβ axis. This study demonstrated a novel biological function of cytoplasmic maspin in progression of breast cancer cells with an aggressive phenotype.Tomohiko SakabeMakoto WakaharaGoshi ShiotaYoshihisa UmekitaNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 11, Iss 1, Pp 1-12 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Tomohiko Sakabe Makoto Wakahara Goshi Shiota Yoshihisa Umekita Role of cytoplasmic localization of maspin in promoting cell invasion in breast cancer with aggressive phenotype
description	Abstract Mammary serine protease inhibitor (maspin) is a tumor suppressor gene that is downregulated during carcinogenesis and breast cancer progression. While the nuclear localization of maspin is essential for tumor suppression, we previously reported that the cytoplasmic localization of maspin was significantly correlated with poor prognosis in breast cancer patients. To understand the mechanisms that underlie oncogenic role of cytoplasmic maspin, we studied its biological function in breast cancer cell lines. Subcellular localization of maspin in MDA-MB-231 breast cancer cells was mainly detected in the cytoplasm, whereas in MCF10A mammary epithelial cells, maspin was present in both cytoplasm and nucleus. In MDA-MB-231 cells, maspin overexpression promoted cell proliferation and cell invasion, whereas maspin downregulation resulted in the opposite effect. Further, we observed that SRGN protein levels were increased in MDA-MB-231 cells stably overexpressing maspin. Finally, maspin overexpression in MDA-MB-231 cells resulted in the N-cadherin and epithelial mesenchymal transition (EMT)-related transcription factors upregulation, and TGFβ signaling pathway activation. These results suggested that cytoplasmic maspin enhances the invasive and metastatic potential in breast cancer cells with aggressive phenotype by inducing EMT via SRGN/TGFβ axis. This study demonstrated a novel biological function of cytoplasmic maspin in progression of breast cancer cells with an aggressive phenotype.
format	article
author	Tomohiko Sakabe Makoto Wakahara Goshi Shiota Yoshihisa Umekita
author_facet	Tomohiko Sakabe Makoto Wakahara Goshi Shiota Yoshihisa Umekita
author_sort	Tomohiko Sakabe
title	Role of cytoplasmic localization of maspin in promoting cell invasion in breast cancer with aggressive phenotype
title_short	Role of cytoplasmic localization of maspin in promoting cell invasion in breast cancer with aggressive phenotype
title_full	Role of cytoplasmic localization of maspin in promoting cell invasion in breast cancer with aggressive phenotype
title_fullStr	Role of cytoplasmic localization of maspin in promoting cell invasion in breast cancer with aggressive phenotype
title_full_unstemmed	Role of cytoplasmic localization of maspin in promoting cell invasion in breast cancer with aggressive phenotype
title_sort	role of cytoplasmic localization of maspin in promoting cell invasion in breast cancer with aggressive phenotype
publisher	Nature Portfolio
publishDate	2021
url	https://doaj.org/article/66d6afc5b65f4960b3332db74bc0a913
work_keys_str_mv	AT tomohikosakabe roleofcytoplasmiclocalizationofmaspininpromotingcellinvasioninbreastcancerwithaggressivephenotype AT makotowakahara roleofcytoplasmiclocalizationofmaspininpromotingcellinvasioninbreastcancerwithaggressivephenotype AT goshishiota roleofcytoplasmiclocalizationofmaspininpromotingcellinvasioninbreastcancerwithaggressivephenotype AT yoshihisaumekita roleofcytoplasmiclocalizationofmaspininpromotingcellinvasioninbreastcancerwithaggressivephenotype
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Role of cytoplasmic localization of maspin in promoting cell invasion in breast cancer with aggressive phenotype

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