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Study on the Function and Mechanism of miR-585-3p Inhibiting the Progression of Ovarian Cancer Cells by Targeting FSCN1 to Block the MAPK Signaling Pathway

Ovarian cancer (OC) is the leading cause of death for women diagnosed with gynecological cancer. Studies have shown that dysregulated miRNA expression is related to various cancers, including OC. Here, we aimed to explore the biological function and mechanism of miR-585-3p in the occurrence and deve...

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Autores principales: Jia, Yiming, Li, Jingru, Wang, Jinfeng, Luo, Tianjiao, Jing, Xiaoqian, Zhao, Hongmin
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Hindawi 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9122712/
https://www.ncbi.nlm.nih.gov/pubmed/35602576
http://dx.doi.org/10.1155/2022/1732365
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author Jia, Yiming
Li, Jingru
Wang, Jinfeng
Luo, Tianjiao
Jing, Xiaoqian
Zhao, Hongmin
author_facet Jia, Yiming
Li, Jingru
Wang, Jinfeng
Luo, Tianjiao
Jing, Xiaoqian
Zhao, Hongmin
author_sort Jia, Yiming
collection PubMed
description Ovarian cancer (OC) is the leading cause of death for women diagnosed with gynecological cancer. Studies have shown that dysregulated miRNA expression is related to various cancers, including OC. Here, we aimed to explore the biological function and mechanism of miR-585-3p in the occurrence and development of OC. The expression level of miR-585-3p was found to be low in OC tissues and cells. We analyzed the biological function of miR-585-3p in OC through in vitro cell experiments. The results indicated that overexpression of miR-585-3p inhibited the proliferation, invasion, and migration of SW626 cells, while low expression of miR-585-3p had the opposite effect in SKOV3 cells. We then screened the target genes of miR-585-3p through miRDB database and detected the expression of target genes in OC cells. FSCN1 was found to be most significantly upregulated in OC cells. Dual-luciferase reporter assays revealed FSCN1 as a potential target of miR-585-3p. Western blot analysis showed that miR-585-3p targeted FSCN1 to inhibit protein phosphorylation of ERK. In vivo animal experiments also confirmed that miR-585-3p targets FSCN1 to inhibit tumor growth and block the MAPK signaling pathway. In summary, miR-585-3p inhibits the proliferation, migration, and invasion of OC cells by targeting FSCN1, and its mechanism of action may be achieved by inhibiting the activation of the MAPK signaling pathway. miR-585-3p may serve as a potential biomarker and therapeutic target for OC.
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spelling pubmed-91227122022-05-21 Study on the Function and Mechanism of miR-585-3p Inhibiting the Progression of Ovarian Cancer Cells by Targeting FSCN1 to Block the MAPK Signaling Pathway Jia, Yiming Li, Jingru Wang, Jinfeng Luo, Tianjiao Jing, Xiaoqian Zhao, Hongmin Anal Cell Pathol (Amst) Research Article Ovarian cancer (OC) is the leading cause of death for women diagnosed with gynecological cancer. Studies have shown that dysregulated miRNA expression is related to various cancers, including OC. Here, we aimed to explore the biological function and mechanism of miR-585-3p in the occurrence and development of OC. The expression level of miR-585-3p was found to be low in OC tissues and cells. We analyzed the biological function of miR-585-3p in OC through in vitro cell experiments. The results indicated that overexpression of miR-585-3p inhibited the proliferation, invasion, and migration of SW626 cells, while low expression of miR-585-3p had the opposite effect in SKOV3 cells. We then screened the target genes of miR-585-3p through miRDB database and detected the expression of target genes in OC cells. FSCN1 was found to be most significantly upregulated in OC cells. Dual-luciferase reporter assays revealed FSCN1 as a potential target of miR-585-3p. Western blot analysis showed that miR-585-3p targeted FSCN1 to inhibit protein phosphorylation of ERK. In vivo animal experiments also confirmed that miR-585-3p targets FSCN1 to inhibit tumor growth and block the MAPK signaling pathway. In summary, miR-585-3p inhibits the proliferation, migration, and invasion of OC cells by targeting FSCN1, and its mechanism of action may be achieved by inhibiting the activation of the MAPK signaling pathway. miR-585-3p may serve as a potential biomarker and therapeutic target for OC. Hindawi 2022-05-13 /pmc/articles/PMC9122712/ /pubmed/35602576 http://dx.doi.org/10.1155/2022/1732365 Text en Copyright © 2022 Yiming Jia et al. https://creativecommons.org/licenses/by/4.0/This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Research Article
Jia, Yiming
Li, Jingru
Wang, Jinfeng
Luo, Tianjiao
Jing, Xiaoqian
Zhao, Hongmin
Study on the Function and Mechanism of miR-585-3p Inhibiting the Progression of Ovarian Cancer Cells by Targeting FSCN1 to Block the MAPK Signaling Pathway
title Study on the Function and Mechanism of miR-585-3p Inhibiting the Progression of Ovarian Cancer Cells by Targeting FSCN1 to Block the MAPK Signaling Pathway
title_full Study on the Function and Mechanism of miR-585-3p Inhibiting the Progression of Ovarian Cancer Cells by Targeting FSCN1 to Block the MAPK Signaling Pathway
title_fullStr Study on the Function and Mechanism of miR-585-3p Inhibiting the Progression of Ovarian Cancer Cells by Targeting FSCN1 to Block the MAPK Signaling Pathway
title_full_unstemmed Study on the Function and Mechanism of miR-585-3p Inhibiting the Progression of Ovarian Cancer Cells by Targeting FSCN1 to Block the MAPK Signaling Pathway
title_short Study on the Function and Mechanism of miR-585-3p Inhibiting the Progression of Ovarian Cancer Cells by Targeting FSCN1 to Block the MAPK Signaling Pathway
title_sort study on the function and mechanism of mir-585-3p inhibiting the progression of ovarian cancer cells by targeting fscn1 to block the mapk signaling pathway
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9122712/
https://www.ncbi.nlm.nih.gov/pubmed/35602576
http://dx.doi.org/10.1155/2022/1732365
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