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Interference with circRNA DOCK1 inhibits hepatocellular carcinoma cell proliferation, invasion and migration by regulating the miR-654-5p/SMAD2 axis

Hepatocellular carcinoma (HCC) is the fourth most common cause of cancer-related death worldwide. The aim of the present study was to discuss the role of circular RNA (circRNA) dedicator of cytokinesis 1 (DOCK1) in HCC and whether it can affect cell proliferation, invasion and migration by regulatin...

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Detalles Bibliográficos
Autores principales: Lu, Yujuan, Zhang, Jingzhi, Wu, Yanhui
Formato: Online Artículo Texto
Lenguaje:English
Publicado: D.A. Spandidos 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8240177/
https://www.ncbi.nlm.nih.gov/pubmed/34184075
http://dx.doi.org/10.3892/mmr.2021.12247
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author Lu, Yujuan
Zhang, Jingzhi
Wu, Yanhui
author_facet Lu, Yujuan
Zhang, Jingzhi
Wu, Yanhui
author_sort Lu, Yujuan
collection PubMed
description Hepatocellular carcinoma (HCC) is the fourth most common cause of cancer-related death worldwide. The aim of the present study was to discuss the role of circular RNA (circRNA) dedicator of cytokinesis 1 (DOCK1) in HCC and whether it can affect cell proliferation, invasion and migration by regulating the microRNA (miR)-654-5p/SMAD2 axis. The expression levels of circRNA DOCK1, miR-654-5p and SMAD2 mRNA in HCC cells and transfected Hep3b cells were detected by reverse transcription-quantitative PCR analysis. SMAD2 protein expression levels in HCC cells and transfected Hep3b cells were analyzed by western blot analysis. The viability, proliferation, migration and invasion of transfected Hep3b cells was in turn detected by Cell Counting Kit-8, clone formation, wound healing and Transwell assays. The interaction of circRNA DOCK1 and miR-654-5p, miR-654-5p and SMAD2 was confirmed by the dual-luciferase reporter assay. As a result, the expression of circRNA DOCK1 and SMAD2 was increased, and miR-654-5p was decreased in HCC cells. circRNA DOCK1 directly targeted to miR-654-5p and miR-654-5p directly targeted to SMAD2. Interference with circRNA DOCK1 inhibited the proliferation, invasion and migration of HCC cells by upregulating miR-654-5p expression. The effects of circRNA DOCK1 knockdown could be partially reversed by transfection with a miR-654-5p inhibitor and SMAD2 overexpression. In conclusion, interference with circRNA DOCK1 inhibited proliferation, invasion and migration of HCC cells by regulating the miR-654-5p/SMAD2 axis.
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spelling pubmed-82401772021-07-12 Interference with circRNA DOCK1 inhibits hepatocellular carcinoma cell proliferation, invasion and migration by regulating the miR-654-5p/SMAD2 axis Lu, Yujuan Zhang, Jingzhi Wu, Yanhui Mol Med Rep Articles Hepatocellular carcinoma (HCC) is the fourth most common cause of cancer-related death worldwide. The aim of the present study was to discuss the role of circular RNA (circRNA) dedicator of cytokinesis 1 (DOCK1) in HCC and whether it can affect cell proliferation, invasion and migration by regulating the microRNA (miR)-654-5p/SMAD2 axis. The expression levels of circRNA DOCK1, miR-654-5p and SMAD2 mRNA in HCC cells and transfected Hep3b cells were detected by reverse transcription-quantitative PCR analysis. SMAD2 protein expression levels in HCC cells and transfected Hep3b cells were analyzed by western blot analysis. The viability, proliferation, migration and invasion of transfected Hep3b cells was in turn detected by Cell Counting Kit-8, clone formation, wound healing and Transwell assays. The interaction of circRNA DOCK1 and miR-654-5p, miR-654-5p and SMAD2 was confirmed by the dual-luciferase reporter assay. As a result, the expression of circRNA DOCK1 and SMAD2 was increased, and miR-654-5p was decreased in HCC cells. circRNA DOCK1 directly targeted to miR-654-5p and miR-654-5p directly targeted to SMAD2. Interference with circRNA DOCK1 inhibited the proliferation, invasion and migration of HCC cells by upregulating miR-654-5p expression. The effects of circRNA DOCK1 knockdown could be partially reversed by transfection with a miR-654-5p inhibitor and SMAD2 overexpression. In conclusion, interference with circRNA DOCK1 inhibited proliferation, invasion and migration of HCC cells by regulating the miR-654-5p/SMAD2 axis. D.A. Spandidos 2021-08 2021-06-25 /pmc/articles/PMC8240177/ /pubmed/34184075 http://dx.doi.org/10.3892/mmr.2021.12247 Text en Copyright: © Lu et al. https://creativecommons.org/licenses/by-nc-nd/4.0/This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License (https://creativecommons.org/licenses/by-nc-nd/4.0/) , which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.
spellingShingle Articles
Lu, Yujuan
Zhang, Jingzhi
Wu, Yanhui
Interference with circRNA DOCK1 inhibits hepatocellular carcinoma cell proliferation, invasion and migration by regulating the miR-654-5p/SMAD2 axis
title Interference with circRNA DOCK1 inhibits hepatocellular carcinoma cell proliferation, invasion and migration by regulating the miR-654-5p/SMAD2 axis
title_full Interference with circRNA DOCK1 inhibits hepatocellular carcinoma cell proliferation, invasion and migration by regulating the miR-654-5p/SMAD2 axis
title_fullStr Interference with circRNA DOCK1 inhibits hepatocellular carcinoma cell proliferation, invasion and migration by regulating the miR-654-5p/SMAD2 axis
title_full_unstemmed Interference with circRNA DOCK1 inhibits hepatocellular carcinoma cell proliferation, invasion and migration by regulating the miR-654-5p/SMAD2 axis
title_short Interference with circRNA DOCK1 inhibits hepatocellular carcinoma cell proliferation, invasion and migration by regulating the miR-654-5p/SMAD2 axis
title_sort interference with circrna dock1 inhibits hepatocellular carcinoma cell proliferation, invasion and migration by regulating the mir-654-5p/smad2 axis
topic Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8240177/
https://www.ncbi.nlm.nih.gov/pubmed/34184075
http://dx.doi.org/10.3892/mmr.2021.12247
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