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CircMUC16 promotes autophagy of epithelial ovarian cancer via interaction with ATG13 and miR-199a

BACKGROUND: Circular RNA (circRNA) has been proven to play a significant role in multiple types of cancer. However, the expression and role of circRNAs in epithelial ovarian cancer (EOC) remains elusive. METHODS: CircRNA and mRNA expression profiles of EOC were screened with sequencing analysis. Gen...

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Autores principales: Gan, Xiaoling, Zhu, Hongtao, Jiang, Xingwei, Obiegbusi, Samuel C., Yong, Min, Long, Xingtao, Hu, Jianguo
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7047414/
https://www.ncbi.nlm.nih.gov/pubmed/32111227
http://dx.doi.org/10.1186/s12943-020-01163-z
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author Gan, Xiaoling
Zhu, Hongtao
Jiang, Xingwei
Obiegbusi, Samuel C.
Yong, Min
Long, Xingtao
Hu, Jianguo
author_facet Gan, Xiaoling
Zhu, Hongtao
Jiang, Xingwei
Obiegbusi, Samuel C.
Yong, Min
Long, Xingtao
Hu, Jianguo
author_sort Gan, Xiaoling
collection PubMed
description BACKGROUND: Circular RNA (circRNA) has been proven to play a significant role in multiple types of cancer. However, the expression and role of circRNAs in epithelial ovarian cancer (EOC) remains elusive. METHODS: CircRNA and mRNA expression profiles of EOC were screened with sequencing analysis. Gene silencing and over-expression were used to study circRNA function. Cell proliferation and Matrigel invasion assays were used to detect cell proliferation and invasion, respectively. The expression of circRNAs, mRNAs and miRNAs was detected using qPCR. The location of circRNAs was detected using FISH. The expression of proteins was detected using western blot and immunohistochemistry. RESULTS: CircMUC16 had increased expression in EOC tissues as compared to healthy ovarian tissues. The expression of circMUC16 was linked to the progression in stage and grade of EOC. Hence, silencing circMUC16 suppressed autophagy flux of SKOV3 cells. In contrast, ectopic expression of circMUC16 promoted autophagy flux of A2780 cells. CircMUC16-mediated autophagy exacerbated EOC invasion and metastasis. Mechanistically, circMUC16 could directly bind to miR-199a-5p and relieve suppression of target Beclin1 and RUNX1. In turn, RUNX1 elevated the expression of circMUC16 via promotion of its transcription. CircMUC16 could directly bind to ATG13 and promote its expression. CONCLUSION: This study demonstrated that circMUC16 regulated Beclin1 and RUNX1 by sponging miR-199a-5p. The data suggested that circMUC16 could be a potential target for EOC diagnosis and therapy.
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spelling pubmed-70474142020-03-03 CircMUC16 promotes autophagy of epithelial ovarian cancer via interaction with ATG13 and miR-199a Gan, Xiaoling Zhu, Hongtao Jiang, Xingwei Obiegbusi, Samuel C. Yong, Min Long, Xingtao Hu, Jianguo Mol Cancer Research BACKGROUND: Circular RNA (circRNA) has been proven to play a significant role in multiple types of cancer. However, the expression and role of circRNAs in epithelial ovarian cancer (EOC) remains elusive. METHODS: CircRNA and mRNA expression profiles of EOC were screened with sequencing analysis. Gene silencing and over-expression were used to study circRNA function. Cell proliferation and Matrigel invasion assays were used to detect cell proliferation and invasion, respectively. The expression of circRNAs, mRNAs and miRNAs was detected using qPCR. The location of circRNAs was detected using FISH. The expression of proteins was detected using western blot and immunohistochemistry. RESULTS: CircMUC16 had increased expression in EOC tissues as compared to healthy ovarian tissues. The expression of circMUC16 was linked to the progression in stage and grade of EOC. Hence, silencing circMUC16 suppressed autophagy flux of SKOV3 cells. In contrast, ectopic expression of circMUC16 promoted autophagy flux of A2780 cells. CircMUC16-mediated autophagy exacerbated EOC invasion and metastasis. Mechanistically, circMUC16 could directly bind to miR-199a-5p and relieve suppression of target Beclin1 and RUNX1. In turn, RUNX1 elevated the expression of circMUC16 via promotion of its transcription. CircMUC16 could directly bind to ATG13 and promote its expression. CONCLUSION: This study demonstrated that circMUC16 regulated Beclin1 and RUNX1 by sponging miR-199a-5p. The data suggested that circMUC16 could be a potential target for EOC diagnosis and therapy. BioMed Central 2020-02-28 /pmc/articles/PMC7047414/ /pubmed/32111227 http://dx.doi.org/10.1186/s12943-020-01163-z Text en © The Author(s) 2020 Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided 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 Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.
spellingShingle Research
Gan, Xiaoling
Zhu, Hongtao
Jiang, Xingwei
Obiegbusi, Samuel C.
Yong, Min
Long, Xingtao
Hu, Jianguo
CircMUC16 promotes autophagy of epithelial ovarian cancer via interaction with ATG13 and miR-199a
title CircMUC16 promotes autophagy of epithelial ovarian cancer via interaction with ATG13 and miR-199a
title_full CircMUC16 promotes autophagy of epithelial ovarian cancer via interaction with ATG13 and miR-199a
title_fullStr CircMUC16 promotes autophagy of epithelial ovarian cancer via interaction with ATG13 and miR-199a
title_full_unstemmed CircMUC16 promotes autophagy of epithelial ovarian cancer via interaction with ATG13 and miR-199a
title_short CircMUC16 promotes autophagy of epithelial ovarian cancer via interaction with ATG13 and miR-199a
title_sort circmuc16 promotes autophagy of epithelial ovarian cancer via interaction with atg13 and mir-199a
topic Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7047414/
https://www.ncbi.nlm.nih.gov/pubmed/32111227
http://dx.doi.org/10.1186/s12943-020-01163-z
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