miR-22 suppresses tumorigenesis and improves radiosensitivity of breast cancer cells by targeting Sirt1

Abstract Background miR-22 has been shown to be frequently downregulated and act as a tumor suppressor in multiple cancers including breast cancers. However, the role of miR-22 in regulating the radioresistance of breast cancer cells, as well as its underlying mechanism is still not well understoo...

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Autores principales:	Zhang,Xia, Li,Yuehua, Wang,Dan, Wei,Xiaoer
Lenguaje:	English
Publicado:	Sociedad de Biología de Chile 2017
Materias:	miR-22 Tumorigenesis Radiosensitivity Breast cancer Sirt1
Acceso en línea:	http://www.scielo.cl/scielo.php?script=sci_arttext&pid=S0716-97602017000100220
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spelling	oai:scielo:S0716-976020170001002202017-11-03miR-22 suppresses tumorigenesis and improves radiosensitivity of breast cancer cells by targeting Sirt1Zhang,XiaLi,YuehuaWang,DanWei,Xiaoer miR-22 Tumorigenesis Radiosensitivity Breast cancer Sirt1 Abstract Background miR-22 has been shown to be frequently downregulated and act as a tumor suppressor in multiple cancers including breast cancers. However, the role of miR-22 in regulating the radioresistance of breast cancer cells, as well as its underlying mechanism is still not well understood. Methods The expressions of miR-22 and sirt1 at mRNA and protein levels were examined by qRT-PCR and Western Blot. The effects of miR-22 overexpression and sirt1 knockdown on cell viability, apoptosis, radiosensitivity, γ-H2AX foci formation were evaluated by CCK-8 assay, flow cytometry, colony formation assay, and γ-H2AX foci formation assay, respectively. Luciferase reporter assay and qRT-PCR analysis were performed to confirm the interaction between miR-22 and sirt1. Results miR-22 was downregulated and sirt1 was upregulated at both mRNA and protein levels in breast cancer cells. miR-22 overexpression or sirt1 knockdown significantly suppressed viability, induced apoptosis, reduced survival fraction, and increased the number of γ-H2AX foci in breast cancer cells. Sirt1 was identified as a target of miR-22 and miR-22 negatively regulated sirt1 expression. Ectopic expression of sirt1 dramatically reversed the inhibitory effect of miR-22 on cell viability and promotive effect on apoptotic rates and radiosensitivity in breast cancer cells. Conclusions miR-22 suppresses tumorigenesis and improves radiosensitivity of breast cancer cells by targeting sirt1, providing a promising therapeutic target for breast cancer.info:eu-repo/semantics/openAccessSociedad de Biología de ChileBiological Research v.50 20172017-01-01text/htmlhttp://www.scielo.cl/scielo.php?script=sci_arttext&pid=S0716-97602017000100220en10.1186/s40659-017-0133-8
institution	Scielo Chile
collection	Scielo Chile
language	English
topic	miR-22 Tumorigenesis Radiosensitivity Breast cancer Sirt1
spellingShingle	miR-22 Tumorigenesis Radiosensitivity Breast cancer Sirt1 Zhang,Xia Li,Yuehua Wang,Dan Wei,Xiaoer miR-22 suppresses tumorigenesis and improves radiosensitivity of breast cancer cells by targeting Sirt1
description	Abstract Background miR-22 has been shown to be frequently downregulated and act as a tumor suppressor in multiple cancers including breast cancers. However, the role of miR-22 in regulating the radioresistance of breast cancer cells, as well as its underlying mechanism is still not well understood. Methods The expressions of miR-22 and sirt1 at mRNA and protein levels were examined by qRT-PCR and Western Blot. The effects of miR-22 overexpression and sirt1 knockdown on cell viability, apoptosis, radiosensitivity, γ-H2AX foci formation were evaluated by CCK-8 assay, flow cytometry, colony formation assay, and γ-H2AX foci formation assay, respectively. Luciferase reporter assay and qRT-PCR analysis were performed to confirm the interaction between miR-22 and sirt1. Results miR-22 was downregulated and sirt1 was upregulated at both mRNA and protein levels in breast cancer cells. miR-22 overexpression or sirt1 knockdown significantly suppressed viability, induced apoptosis, reduced survival fraction, and increased the number of γ-H2AX foci in breast cancer cells. Sirt1 was identified as a target of miR-22 and miR-22 negatively regulated sirt1 expression. Ectopic expression of sirt1 dramatically reversed the inhibitory effect of miR-22 on cell viability and promotive effect on apoptotic rates and radiosensitivity in breast cancer cells. Conclusions miR-22 suppresses tumorigenesis and improves radiosensitivity of breast cancer cells by targeting sirt1, providing a promising therapeutic target for breast cancer.
author	Zhang,Xia Li,Yuehua Wang,Dan Wei,Xiaoer
author_facet	Zhang,Xia Li,Yuehua Wang,Dan Wei,Xiaoer
author_sort	Zhang,Xia
title	miR-22 suppresses tumorigenesis and improves radiosensitivity of breast cancer cells by targeting Sirt1
title_short	miR-22 suppresses tumorigenesis and improves radiosensitivity of breast cancer cells by targeting Sirt1
title_full	miR-22 suppresses tumorigenesis and improves radiosensitivity of breast cancer cells by targeting Sirt1
title_fullStr	miR-22 suppresses tumorigenesis and improves radiosensitivity of breast cancer cells by targeting Sirt1
title_full_unstemmed	miR-22 suppresses tumorigenesis and improves radiosensitivity of breast cancer cells by targeting Sirt1
title_sort	mir-22 suppresses tumorigenesis and improves radiosensitivity of breast cancer cells by targeting sirt1
publisher	Sociedad de Biología de Chile
publishDate	2017
url	http://www.scielo.cl/scielo.php?script=sci_arttext&pid=S0716-97602017000100220
work_keys_str_mv	AT zhangxia mir22suppressestumorigenesisandimprovesradiosensitivityofbreastcancercellsbytargetingsirt1 AT liyuehua mir22suppressestumorigenesisandimprovesradiosensitivityofbreastcancercellsbytargetingsirt1 AT wangdan mir22suppressestumorigenesisandimprovesradiosensitivityofbreastcancercellsbytargetingsirt1 AT weixiaoer mir22suppressestumorigenesisandimprovesradiosensitivityofbreastcancercellsbytargetingsirt1
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miR-22 suppresses tumorigenesis and improves radiosensitivity of breast cancer cells by targeting Sirt1

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