The MIRNA mir-582-3p suppresses ovarian cancer progression by targeting AKT/MTOR signaling via lncRNA TUG1

Ovarian cancer (OC) is one of the most common malignancies of the female reproductive system. The miRNA miR-582-3p is associated with a variety of tumors, and the aim of this study was to investigate the role and mechanisms of miR-582-3p specifically in ovarian carcinogenesis and progression. Low ex...

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Autores principales:	Tianyu Dai, Junhui Liang, Wei Liu, Yonghui Zou, Feifei Niu, Mengqing Li, Haomeng Zhang, Changzhong Li, Mingjun Fan, Guoying Cui
Formato:	article
Lenguaje:	EN
Publicado:	Taylor & Francis Group 2021
Materias:	mir-582-3p ovarian cancer lncrna tug1 akt/mtor signaling pathway Biotechnology TP248.13-248.65
Acceso en línea:	https://doaj.org/article/0ef39530e11c4874ad16bd1bb1bfb80e
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spelling	oai:doaj.org-article:0ef39530e11c4874ad16bd1bb1bfb80e2021-11-26T11:19:49ZThe MIRNA mir-582-3p suppresses ovarian cancer progression by targeting AKT/MTOR signaling via lncRNA TUG12165-59792165-598710.1080/21655979.2021.2003662https://doaj.org/article/0ef39530e11c4874ad16bd1bb1bfb80e2021-11-01T00:00:00Zhttp://dx.doi.org/10.1080/21655979.2021.2003662https://doaj.org/toc/2165-5979https://doaj.org/toc/2165-5987Ovarian cancer (OC) is one of the most common malignancies of the female reproductive system. The miRNA miR-582-3p is associated with a variety of tumors, and the aim of this study was to investigate the role and mechanisms of miR-582-3p specifically in ovarian carcinogenesis and progression. Low expression of miR-582-3p was noted in OC tissue and cell lines, and lower expression of miR-582-3p correlated with lower overall survival in OC patients. Knockdown of miR-582-3p promoted the proliferation and migration of OC cells, while overexpression inhibited them. TUG1, a long non-coding RNA, was found to bind to miR-582-3p, and inhibition of lncRNA TUG1 decreased viability and migration and weakened the effect of miR-582-3p knockdown in OC cells. Implantation of OC cells with reduced miR-582-3p caused increased tumor growth, while lncRNA TUG1 knockdown suppressed tumor growth and relieved the impact of reduced miR-582-3p in vivo. Phosphorylation of AKT and mTOR were significantly enhanced with decreased miR-582-3p expression, but lncRNA TUG1 knockdown attenuated this trend in vitro and in vivo. The novel miR-582-3p represses the malignant properties of OC via the AKT/mTOR signaling pathway by targeting lncRNA TUG1. This axis may represent valuable prognostic biomarkers and therapeutic targets for OC.Tianyu DaiJunhui LiangWei LiuYonghui ZouFeifei NiuMengqing LiHaomeng ZhangChangzhong LiMingjun FanGuoying CuiTaylor & Francis Grouparticlemir-582-3povarian cancerlncrna tug1akt/mtor signaling pathwayBiotechnologyTP248.13-248.65ENBioengineered, Vol 0, Iss 0 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	mir-582-3p ovarian cancer lncrna tug1 akt/mtor signaling pathway Biotechnology TP248.13-248.65
spellingShingle	mir-582-3p ovarian cancer lncrna tug1 akt/mtor signaling pathway Biotechnology TP248.13-248.65 Tianyu Dai Junhui Liang Wei Liu Yonghui Zou Feifei Niu Mengqing Li Haomeng Zhang Changzhong Li Mingjun Fan Guoying Cui The MIRNA mir-582-3p suppresses ovarian cancer progression by targeting AKT/MTOR signaling via lncRNA TUG1
description	Ovarian cancer (OC) is one of the most common malignancies of the female reproductive system. The miRNA miR-582-3p is associated with a variety of tumors, and the aim of this study was to investigate the role and mechanisms of miR-582-3p specifically in ovarian carcinogenesis and progression. Low expression of miR-582-3p was noted in OC tissue and cell lines, and lower expression of miR-582-3p correlated with lower overall survival in OC patients. Knockdown of miR-582-3p promoted the proliferation and migration of OC cells, while overexpression inhibited them. TUG1, a long non-coding RNA, was found to bind to miR-582-3p, and inhibition of lncRNA TUG1 decreased viability and migration and weakened the effect of miR-582-3p knockdown in OC cells. Implantation of OC cells with reduced miR-582-3p caused increased tumor growth, while lncRNA TUG1 knockdown suppressed tumor growth and relieved the impact of reduced miR-582-3p in vivo. Phosphorylation of AKT and mTOR were significantly enhanced with decreased miR-582-3p expression, but lncRNA TUG1 knockdown attenuated this trend in vitro and in vivo. The novel miR-582-3p represses the malignant properties of OC via the AKT/mTOR signaling pathway by targeting lncRNA TUG1. This axis may represent valuable prognostic biomarkers and therapeutic targets for OC.
format	article
author	Tianyu Dai Junhui Liang Wei Liu Yonghui Zou Feifei Niu Mengqing Li Haomeng Zhang Changzhong Li Mingjun Fan Guoying Cui
author_facet	Tianyu Dai Junhui Liang Wei Liu Yonghui Zou Feifei Niu Mengqing Li Haomeng Zhang Changzhong Li Mingjun Fan Guoying Cui
author_sort	Tianyu Dai
title	The MIRNA mir-582-3p suppresses ovarian cancer progression by targeting AKT/MTOR signaling via lncRNA TUG1
title_short	The MIRNA mir-582-3p suppresses ovarian cancer progression by targeting AKT/MTOR signaling via lncRNA TUG1
title_full	The MIRNA mir-582-3p suppresses ovarian cancer progression by targeting AKT/MTOR signaling via lncRNA TUG1
title_fullStr	The MIRNA mir-582-3p suppresses ovarian cancer progression by targeting AKT/MTOR signaling via lncRNA TUG1
title_full_unstemmed	The MIRNA mir-582-3p suppresses ovarian cancer progression by targeting AKT/MTOR signaling via lncRNA TUG1
title_sort	mirna mir-582-3p suppresses ovarian cancer progression by targeting akt/mtor signaling via lncrna tug1
publisher	Taylor & Francis Group
publishDate	2021
url	https://doaj.org/article/0ef39530e11c4874ad16bd1bb1bfb80e
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The MIRNA mir-582-3p suppresses ovarian cancer progression by targeting AKT/MTOR signaling via lncRNA TUG1

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