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The LINC00922 aggravates ovarian cancer progression via sponging miR-361-3p
BACKGROUND: Long noncoding RNA (lncRNA) LINC00922 has been reported to promote tumorigenesis of lung and breast cancer. However, the functions and mechanisms of LINC00922 in ovarian cancer (OC) remain unclarified. The current study aims to clarify the detailed functions and underlying mechanisms of...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
BioMed Central
2021
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8194245/ https://www.ncbi.nlm.nih.gov/pubmed/34116704 http://dx.doi.org/10.1186/s13048-021-00828-7 |
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author | Wang, Liping Ren, Chenchen Xu, Yajuan Yang, Li Chen, Yannan Zhu, Yuanhang |
author_facet | Wang, Liping Ren, Chenchen Xu, Yajuan Yang, Li Chen, Yannan Zhu, Yuanhang |
author_sort | Wang, Liping |
collection | PubMed |
description | BACKGROUND: Long noncoding RNA (lncRNA) LINC00922 has been reported to promote tumorigenesis of lung and breast cancer. However, the functions and mechanisms of LINC00922 in ovarian cancer (OC) remain unclarified. The current study aims to clarify the detailed functions and underlying mechanisms of LINC00922 in the progression of OC. METHODS: LINC00922 expression in OC tissues and cells was identified by a comprehensive strategy of data miming, computational biology and quantitative real-time polymerase chain reaction (RT-qPCR) experiment. In vitro CCK-8, wound healing, transwell invasion, western blotting and in vivo tumorigenesis assays LINC00922 were conducted to evaluate the functions of LINC00992. Subsequently, bioinformatics technology and dual luciferase reporter assay were performed to confirm the between miR-361-3p and LINC00922 or CLDN1. Finally, rescue experiments were performed to confirm whether LINC00922 effect functions of OC cells through regulation of miR-361-3p. RESULTS: LINC00922 was significantly upregulated in OC tissues and cell lines, which is significantly positively corelated with the poor prognosis of patients with OC. LINC00922 knockdown inhibited proliferation and tumorigenesis of OC cells in vitro and vivo. In addition, LINC00922 knockdown suppressed migration, invasion, and EMT of OC cells in vitro. Mechanically, LINC00922 could competitively bind with miR-361-3p to relieve the repressive effect of miR-361-3p on its target gene CLDN1 in OC cells. In addition, silencing miR-361-3p promoted OC cell proliferation, migration, invasion, EMT and Wnt/β-catenin signaling, while LINC00922 knockdown inhibited Wnt/β-catenin signaling by upregulating miR-361-3p. Rescue experiments revealed that LINC00922 knockdown inhibited OC cell proliferation, migration, invasion and EMT by regulating miR-361-3p. CONCLUSION: This study suggested that LINC00922 could competitively bind with miR-361-3p to promote the CLDN1 expression and activate Wnt/β-catenin signaling in OC progression, which providing a promising therapeutically target for OC. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1186/s13048-021-00828-7. |
format | Online Article Text |
id | pubmed-8194245 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-81942452021-06-15 The LINC00922 aggravates ovarian cancer progression via sponging miR-361-3p Wang, Liping Ren, Chenchen Xu, Yajuan Yang, Li Chen, Yannan Zhu, Yuanhang J Ovarian Res Research BACKGROUND: Long noncoding RNA (lncRNA) LINC00922 has been reported to promote tumorigenesis of lung and breast cancer. However, the functions and mechanisms of LINC00922 in ovarian cancer (OC) remain unclarified. The current study aims to clarify the detailed functions and underlying mechanisms of LINC00922 in the progression of OC. METHODS: LINC00922 expression in OC tissues and cells was identified by a comprehensive strategy of data miming, computational biology and quantitative real-time polymerase chain reaction (RT-qPCR) experiment. In vitro CCK-8, wound healing, transwell invasion, western blotting and in vivo tumorigenesis assays LINC00922 were conducted to evaluate the functions of LINC00992. Subsequently, bioinformatics technology and dual luciferase reporter assay were performed to confirm the between miR-361-3p and LINC00922 or CLDN1. Finally, rescue experiments were performed to confirm whether LINC00922 effect functions of OC cells through regulation of miR-361-3p. RESULTS: LINC00922 was significantly upregulated in OC tissues and cell lines, which is significantly positively corelated with the poor prognosis of patients with OC. LINC00922 knockdown inhibited proliferation and tumorigenesis of OC cells in vitro and vivo. In addition, LINC00922 knockdown suppressed migration, invasion, and EMT of OC cells in vitro. Mechanically, LINC00922 could competitively bind with miR-361-3p to relieve the repressive effect of miR-361-3p on its target gene CLDN1 in OC cells. In addition, silencing miR-361-3p promoted OC cell proliferation, migration, invasion, EMT and Wnt/β-catenin signaling, while LINC00922 knockdown inhibited Wnt/β-catenin signaling by upregulating miR-361-3p. Rescue experiments revealed that LINC00922 knockdown inhibited OC cell proliferation, migration, invasion and EMT by regulating miR-361-3p. CONCLUSION: This study suggested that LINC00922 could competitively bind with miR-361-3p to promote the CLDN1 expression and activate Wnt/β-catenin signaling in OC progression, which providing a promising therapeutically target for OC. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1186/s13048-021-00828-7. BioMed Central 2021-06-11 /pmc/articles/PMC8194245/ /pubmed/34116704 http://dx.doi.org/10.1186/s13048-021-00828-7 Text en © The Author(s) 2021 https://creativecommons.org/licenses/by/4.0/Open AccessThis 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 licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence 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 licence, visit http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) . The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/ (https://creativecommons.org/publicdomain/zero/1.0/) ) applies to the data made available in this article, unless otherwise stated in a credit line to the data. |
spellingShingle | Research Wang, Liping Ren, Chenchen Xu, Yajuan Yang, Li Chen, Yannan Zhu, Yuanhang The LINC00922 aggravates ovarian cancer progression via sponging miR-361-3p |
title | The LINC00922 aggravates ovarian cancer progression via sponging miR-361-3p |
title_full | The LINC00922 aggravates ovarian cancer progression via sponging miR-361-3p |
title_fullStr | The LINC00922 aggravates ovarian cancer progression via sponging miR-361-3p |
title_full_unstemmed | The LINC00922 aggravates ovarian cancer progression via sponging miR-361-3p |
title_short | The LINC00922 aggravates ovarian cancer progression via sponging miR-361-3p |
title_sort | linc00922 aggravates ovarian cancer progression via sponging mir-361-3p |
topic | Research |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8194245/ https://www.ncbi.nlm.nih.gov/pubmed/34116704 http://dx.doi.org/10.1186/s13048-021-00828-7 |
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