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Catalpol inhibits the proliferation, migration and metastasis of HCC cells by regulating miR-140-5p expression

Hepatocellular carcinoma (HCC) is a frequent malignant tumor. Catalpol is a Chinese medicine extract with a number of pharmacologically active properties. The present study aimed to investigate the effects and mechanisms of catalpol in HCC. HCC cells were treated with catalpol in the presence or abs...

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Autores principales: Wu, Linsheng, Li, Haoxia, Chen, Shengyou, Wu, Xiaoqiang, Chen, Xiaomin, Wang, Fangping
Formato: Online Artículo Texto
Lenguaje:English
Publicado: D.A. Spandidos 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7673346/
https://www.ncbi.nlm.nih.gov/pubmed/33179108
http://dx.doi.org/10.3892/mmr.2020.11667
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author Wu, Linsheng
Li, Haoxia
Chen, Shengyou
Wu, Xiaoqiang
Chen, Xiaomin
Wang, Fangping
author_facet Wu, Linsheng
Li, Haoxia
Chen, Shengyou
Wu, Xiaoqiang
Chen, Xiaomin
Wang, Fangping
author_sort Wu, Linsheng
collection PubMed
description Hepatocellular carcinoma (HCC) is a frequent malignant tumor. Catalpol is a Chinese medicine extract with a number of pharmacologically active properties. The present study aimed to investigate the effects and mechanisms of catalpol in HCC. HCC cells were treated with catalpol in the presence or absence of microRNA (miR)-140-5p inhibitor, and assays to determine cell viability, proliferation, invasion and migration were performed. Reverse transcription-quantitative PCR and western blotting were performed to determine the mRNA and protein expression levels of miR-140-5p, vimentin, N-Cadherin and E-Cadherin. Moreover, cells were treated with catalpol in the absence or presence of transforming growth factor (TGF)-β1, and the cell morphology was observed under a microscope. The results demonstrated that catalpol inhibited cell proliferation, invasion and migration, and decreased the expression levels of vimentin and N-cadherin, but increased the expression levels of E-cadherin and miR-140-5p. Catalpol inhibited morphological changes in epithelial-mesenchymal transformation (EMT) of cells induced by TGF-β1. Following inhibition of miR-140-5p expression, the proliferation, invasion and migration of HCC cells were promoted, E-cadherin expression was decreased, and the levels of vimentin and N-cadherin were increased. The miR-140-5p inhibitor effectively reversed the inhibitory effect of catalpol on cell proliferation, invasion and migration. Thus, the results suggested that the antitumor potential of catalpol in HCC may be exerted by regulating the expression of miR-140-5p to inhibit proliferation, invasion, migration and EMT of HCC cells.
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spelling pubmed-76733462020-11-20 Catalpol inhibits the proliferation, migration and metastasis of HCC cells by regulating miR-140-5p expression Wu, Linsheng Li, Haoxia Chen, Shengyou Wu, Xiaoqiang Chen, Xiaomin Wang, Fangping Mol Med Rep Articles Hepatocellular carcinoma (HCC) is a frequent malignant tumor. Catalpol is a Chinese medicine extract with a number of pharmacologically active properties. The present study aimed to investigate the effects and mechanisms of catalpol in HCC. HCC cells were treated with catalpol in the presence or absence of microRNA (miR)-140-5p inhibitor, and assays to determine cell viability, proliferation, invasion and migration were performed. Reverse transcription-quantitative PCR and western blotting were performed to determine the mRNA and protein expression levels of miR-140-5p, vimentin, N-Cadherin and E-Cadherin. Moreover, cells were treated with catalpol in the absence or presence of transforming growth factor (TGF)-β1, and the cell morphology was observed under a microscope. The results demonstrated that catalpol inhibited cell proliferation, invasion and migration, and decreased the expression levels of vimentin and N-cadherin, but increased the expression levels of E-cadherin and miR-140-5p. Catalpol inhibited morphological changes in epithelial-mesenchymal transformation (EMT) of cells induced by TGF-β1. Following inhibition of miR-140-5p expression, the proliferation, invasion and migration of HCC cells were promoted, E-cadherin expression was decreased, and the levels of vimentin and N-cadherin were increased. The miR-140-5p inhibitor effectively reversed the inhibitory effect of catalpol on cell proliferation, invasion and migration. Thus, the results suggested that the antitumor potential of catalpol in HCC may be exerted by regulating the expression of miR-140-5p to inhibit proliferation, invasion, migration and EMT of HCC cells. D.A. Spandidos 2021-01 2020-11-04 /pmc/articles/PMC7673346/ /pubmed/33179108 http://dx.doi.org/10.3892/mmr.2020.11667 Text en Copyright: © Wu et al. 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
Wu, Linsheng
Li, Haoxia
Chen, Shengyou
Wu, Xiaoqiang
Chen, Xiaomin
Wang, Fangping
Catalpol inhibits the proliferation, migration and metastasis of HCC cells by regulating miR-140-5p expression
title Catalpol inhibits the proliferation, migration and metastasis of HCC cells by regulating miR-140-5p expression
title_full Catalpol inhibits the proliferation, migration and metastasis of HCC cells by regulating miR-140-5p expression
title_fullStr Catalpol inhibits the proliferation, migration and metastasis of HCC cells by regulating miR-140-5p expression
title_full_unstemmed Catalpol inhibits the proliferation, migration and metastasis of HCC cells by regulating miR-140-5p expression
title_short Catalpol inhibits the proliferation, migration and metastasis of HCC cells by regulating miR-140-5p expression
title_sort catalpol inhibits the proliferation, migration and metastasis of hcc cells by regulating mir-140-5p expression
topic Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7673346/
https://www.ncbi.nlm.nih.gov/pubmed/33179108
http://dx.doi.org/10.3892/mmr.2020.11667
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