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Circular RNA circEXOC6B Inhibits the Progression of Ovarian Cancer by Sponging miR-421 and Regulating RUS1 Expression

BACKGROUND: Evidence has been shown that circular RNAs (circRNAs) play a vital role during the development of ovarian cancer. However, the mechanism by which circEXOC6B regulates tumorigenesis of ovarian cancer remains unknown. Thus, this study aimed to investigate the role of circEXOC6B during the...

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Autores principales: Wang, Zhonghai, Zhang, Wenmin, Fang, Jinchuan, Xie, Ping, Miao, Miao, Yang, Hongwen
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Dove 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7443403/
https://www.ncbi.nlm.nih.gov/pubmed/32884301
http://dx.doi.org/10.2147/OTT.S243040
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author Wang, Zhonghai
Zhang, Wenmin
Fang, Jinchuan
Xie, Ping
Miao, Miao
Yang, Hongwen
author_facet Wang, Zhonghai
Zhang, Wenmin
Fang, Jinchuan
Xie, Ping
Miao, Miao
Yang, Hongwen
author_sort Wang, Zhonghai
collection PubMed
description BACKGROUND: Evidence has been shown that circular RNAs (circRNAs) play a vital role during the development of ovarian cancer. However, the mechanism by which circEXOC6B regulates tumorigenesis of ovarian cancer remains unknown. Thus, this study aimed to investigate the role of circEXOC6B during the progression of ovarian cancer. MATERIALS AND METHODS: The dual-luciferase reporter system assay was used to determine the interaction between circEXOC6B, miR-421 and RUS1 in ovarian cancer, respectively. CCK8 and colony formatting were used to evaluate cell proliferation. Meanwhile, the expressions of RSU1, PINCH1 and ILK in SKOV3 cells were detected with Western blot. RESULTS: Downregulation of circEXOC6B markedly promoted the proliferation and invasion in A2780 cells. In contrast, upregulation of circEXOC6B significantly inhibited the proliferation and invasion in SKOV3 cells. Moreover, overexpression of circEXOC6B obviously induced the apoptosis of SKOV3 cells. Furthermore, luciferase reporter assay identified that miR-421 was the potential miRNA binding of circEXOC6B, and RUS1 was the potential binding target of miR-421. Mechanism analysis indicated that upregulation of circEXOC6B increased the level of RUS1 by acting as a competitive “sponge” of miR‐421. CONCLUSION: In this study, we found that circEXOC6B suppressed the growth of ovarian cancer cells through upregulating RSU1 partially via sponging miR-421. Therefore, circEXOC6B might be a potential target for the treatment of ovarian cancer.
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spelling pubmed-74434032020-09-02 Circular RNA circEXOC6B Inhibits the Progression of Ovarian Cancer by Sponging miR-421 and Regulating RUS1 Expression Wang, Zhonghai Zhang, Wenmin Fang, Jinchuan Xie, Ping Miao, Miao Yang, Hongwen Onco Targets Ther Original Research BACKGROUND: Evidence has been shown that circular RNAs (circRNAs) play a vital role during the development of ovarian cancer. However, the mechanism by which circEXOC6B regulates tumorigenesis of ovarian cancer remains unknown. Thus, this study aimed to investigate the role of circEXOC6B during the progression of ovarian cancer. MATERIALS AND METHODS: The dual-luciferase reporter system assay was used to determine the interaction between circEXOC6B, miR-421 and RUS1 in ovarian cancer, respectively. CCK8 and colony formatting were used to evaluate cell proliferation. Meanwhile, the expressions of RSU1, PINCH1 and ILK in SKOV3 cells were detected with Western blot. RESULTS: Downregulation of circEXOC6B markedly promoted the proliferation and invasion in A2780 cells. In contrast, upregulation of circEXOC6B significantly inhibited the proliferation and invasion in SKOV3 cells. Moreover, overexpression of circEXOC6B obviously induced the apoptosis of SKOV3 cells. Furthermore, luciferase reporter assay identified that miR-421 was the potential miRNA binding of circEXOC6B, and RUS1 was the potential binding target of miR-421. Mechanism analysis indicated that upregulation of circEXOC6B increased the level of RUS1 by acting as a competitive “sponge” of miR‐421. CONCLUSION: In this study, we found that circEXOC6B suppressed the growth of ovarian cancer cells through upregulating RSU1 partially via sponging miR-421. Therefore, circEXOC6B might be a potential target for the treatment of ovarian cancer. Dove 2020-08-19 /pmc/articles/PMC7443403/ /pubmed/32884301 http://dx.doi.org/10.2147/OTT.S243040 Text en © 2020 Wang et al. http://creativecommons.org/licenses/by-nc/3.0/ This work is published and licensed by Dove Medical Press Limited. The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License (http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. For permission for commercial use of this work, please see paragraphs 4.2 and 5 of our Terms (https://www.dovepress.com/terms.php).
spellingShingle Original Research
Wang, Zhonghai
Zhang, Wenmin
Fang, Jinchuan
Xie, Ping
Miao, Miao
Yang, Hongwen
Circular RNA circEXOC6B Inhibits the Progression of Ovarian Cancer by Sponging miR-421 and Regulating RUS1 Expression
title Circular RNA circEXOC6B Inhibits the Progression of Ovarian Cancer by Sponging miR-421 and Regulating RUS1 Expression
title_full Circular RNA circEXOC6B Inhibits the Progression of Ovarian Cancer by Sponging miR-421 and Regulating RUS1 Expression
title_fullStr Circular RNA circEXOC6B Inhibits the Progression of Ovarian Cancer by Sponging miR-421 and Regulating RUS1 Expression
title_full_unstemmed Circular RNA circEXOC6B Inhibits the Progression of Ovarian Cancer by Sponging miR-421 and Regulating RUS1 Expression
title_short Circular RNA circEXOC6B Inhibits the Progression of Ovarian Cancer by Sponging miR-421 and Regulating RUS1 Expression
title_sort circular rna circexoc6b inhibits the progression of ovarian cancer by sponging mir-421 and regulating rus1 expression
topic Original Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7443403/
https://www.ncbi.nlm.nih.gov/pubmed/32884301
http://dx.doi.org/10.2147/OTT.S243040
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