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Long non-coding RNA SNHG10 upregulates BIN1 to suppress the tumorigenesis and epithelial–mesenchymal transition of epithelial ovarian cancer via sponging miR-200a-3p

Epithelial ovarian cancer (EOC) is one of the most frequent and fatal gynecologic malignant tumors resulting in an unsatisfying prognosis. Long non-coding RNAs (lncRNAs) play pivotal roles in the tumorigenesis and progression of EOC. However, the profile of lncRNAs involved in EOC remains to be expa...

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Autores principales: Lv, Wei, Jia, Yunlong, Wang, Jiali, Duan, Yuqing, Wang, Xuexiao, Liu, Tianxu, Hao, Shuwei, Liu, Lihua
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Nature Publishing Group UK 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8837780/
https://www.ncbi.nlm.nih.gov/pubmed/35149697
http://dx.doi.org/10.1038/s41420-022-00825-9
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author Lv, Wei
Jia, Yunlong
Wang, Jiali
Duan, Yuqing
Wang, Xuexiao
Liu, Tianxu
Hao, Shuwei
Liu, Lihua
author_facet Lv, Wei
Jia, Yunlong
Wang, Jiali
Duan, Yuqing
Wang, Xuexiao
Liu, Tianxu
Hao, Shuwei
Liu, Lihua
author_sort Lv, Wei
collection PubMed
description Epithelial ovarian cancer (EOC) is one of the most frequent and fatal gynecologic malignant tumors resulting in an unsatisfying prognosis. Long non-coding RNAs (lncRNAs) play pivotal roles in the tumorigenesis and progression of EOC. However, the profile of lncRNAs involved in EOC remains to be expanded to further improve clinical treatment strategy. In present study, we identified a novel tumor-suppressive lncRNA small nucleolar RNA host gene 10 (SNHG10) in EOC. Kaplan–Meier analysis and COX proportional hazard progression model showed that low expression of SNHG10 was correlated with a poor prognosis of EOC patients. Overexpressing SNHG10 suppressed the proliferation, colony formation, migration, and invasion of EOC cells. Furthermore, SNHG10 was predicted to sponge miR-200a-3p in EOC cells according to the LncBase v.2 experimental module. Then, the binding of SNHG10 and miR-200a-3p was confirmed by performing quantitative real-time PCR (qRT-PCR) and luciferase reporter assays. RNA immunoprecipitation (RIP) showed that SNHG10 and miR-200a-3p occupied the same Ago2 protein to form an RNA-induced silencing complex (RISC). By overlapping the results from the bioinformatics algorithms, tumor-suppressor bridging integrator-1 (BIN1) was found to be a main downstream target of the SNHG10/miR-200a-3p axis. Low expression of BIN1 in EOC tissues was detected by using immunohistochemistry (IHC). Besides, BIN1 and SNHG10 expression was positively correlated in EOC tissues. By performing miRNA rescue experiments, a SNHG10/miR-200a-3p/BIN1 axis and its promoting effects on malignant behaviors and epithelial–mesenchymal transition (EMT) process were verified in EOC cells. Moreover, SNHG10 overexpression significantly suppressed the tumorigenesis and EMT of EOC cells in vivo. Altogether, SNHG10 sponges miR-200a-3p to upregulate BIN1 and thereby exerting its tumor-suppressive effects in EOC. Therefore, the SNHG10/miR-200a-3p/BIN1 axis may act as a potential predictive biomarker and therapeutic target for treating EOC.
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spelling pubmed-88377802022-03-02 Long non-coding RNA SNHG10 upregulates BIN1 to suppress the tumorigenesis and epithelial–mesenchymal transition of epithelial ovarian cancer via sponging miR-200a-3p Lv, Wei Jia, Yunlong Wang, Jiali Duan, Yuqing Wang, Xuexiao Liu, Tianxu Hao, Shuwei Liu, Lihua Cell Death Discov Article Epithelial ovarian cancer (EOC) is one of the most frequent and fatal gynecologic malignant tumors resulting in an unsatisfying prognosis. Long non-coding RNAs (lncRNAs) play pivotal roles in the tumorigenesis and progression of EOC. However, the profile of lncRNAs involved in EOC remains to be expanded to further improve clinical treatment strategy. In present study, we identified a novel tumor-suppressive lncRNA small nucleolar RNA host gene 10 (SNHG10) in EOC. Kaplan–Meier analysis and COX proportional hazard progression model showed that low expression of SNHG10 was correlated with a poor prognosis of EOC patients. Overexpressing SNHG10 suppressed the proliferation, colony formation, migration, and invasion of EOC cells. Furthermore, SNHG10 was predicted to sponge miR-200a-3p in EOC cells according to the LncBase v.2 experimental module. Then, the binding of SNHG10 and miR-200a-3p was confirmed by performing quantitative real-time PCR (qRT-PCR) and luciferase reporter assays. RNA immunoprecipitation (RIP) showed that SNHG10 and miR-200a-3p occupied the same Ago2 protein to form an RNA-induced silencing complex (RISC). By overlapping the results from the bioinformatics algorithms, tumor-suppressor bridging integrator-1 (BIN1) was found to be a main downstream target of the SNHG10/miR-200a-3p axis. Low expression of BIN1 in EOC tissues was detected by using immunohistochemistry (IHC). Besides, BIN1 and SNHG10 expression was positively correlated in EOC tissues. By performing miRNA rescue experiments, a SNHG10/miR-200a-3p/BIN1 axis and its promoting effects on malignant behaviors and epithelial–mesenchymal transition (EMT) process were verified in EOC cells. Moreover, SNHG10 overexpression significantly suppressed the tumorigenesis and EMT of EOC cells in vivo. Altogether, SNHG10 sponges miR-200a-3p to upregulate BIN1 and thereby exerting its tumor-suppressive effects in EOC. Therefore, the SNHG10/miR-200a-3p/BIN1 axis may act as a potential predictive biomarker and therapeutic target for treating EOC. Nature Publishing Group UK 2022-02-11 /pmc/articles/PMC8837780/ /pubmed/35149697 http://dx.doi.org/10.1038/s41420-022-00825-9 Text en © The Author(s) 2022 https://creativecommons.org/licenses/by/4.0/Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) .
spellingShingle Article
Lv, Wei
Jia, Yunlong
Wang, Jiali
Duan, Yuqing
Wang, Xuexiao
Liu, Tianxu
Hao, Shuwei
Liu, Lihua
Long non-coding RNA SNHG10 upregulates BIN1 to suppress the tumorigenesis and epithelial–mesenchymal transition of epithelial ovarian cancer via sponging miR-200a-3p
title Long non-coding RNA SNHG10 upregulates BIN1 to suppress the tumorigenesis and epithelial–mesenchymal transition of epithelial ovarian cancer via sponging miR-200a-3p
title_full Long non-coding RNA SNHG10 upregulates BIN1 to suppress the tumorigenesis and epithelial–mesenchymal transition of epithelial ovarian cancer via sponging miR-200a-3p
title_fullStr Long non-coding RNA SNHG10 upregulates BIN1 to suppress the tumorigenesis and epithelial–mesenchymal transition of epithelial ovarian cancer via sponging miR-200a-3p
title_full_unstemmed Long non-coding RNA SNHG10 upregulates BIN1 to suppress the tumorigenesis and epithelial–mesenchymal transition of epithelial ovarian cancer via sponging miR-200a-3p
title_short Long non-coding RNA SNHG10 upregulates BIN1 to suppress the tumorigenesis and epithelial–mesenchymal transition of epithelial ovarian cancer via sponging miR-200a-3p
title_sort long non-coding rna snhg10 upregulates bin1 to suppress the tumorigenesis and epithelial–mesenchymal transition of epithelial ovarian cancer via sponging mir-200a-3p
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8837780/
https://www.ncbi.nlm.nih.gov/pubmed/35149697
http://dx.doi.org/10.1038/s41420-022-00825-9
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