MiRNA-200b reverses drug resistance of hepatocellular carcinoma HepG2 cells to sorafenib and its underlying mechanism

Objective To explore the effect of miRNA-200b on sorafenib resistance in hepatocellular carcinoma cells in order to increase the efficacy of the drug in advanced liver cancer patients. Methods Sorafenib resistant hepatocellular carcinoma HepG2-SR cell line was established by gradually increasing th...

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Autores principales: DENG Yong, TANG Tengqian, ZHANG Leida
Formato: article
Lenguaje:ZH
Publicado: Editorial Office of Journal of Third Military Medical University 2021
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spelling oai:doaj.org-article:ebebf18ffa6548c1a4574feac02cd3e22021-11-28T10:47:47ZMiRNA-200b reverses drug resistance of hepatocellular carcinoma HepG2 cells to sorafenib and its underlying mechanism10.16016/j.1000-5404.2021050851000-5404https://doaj.org/article/ebebf18ffa6548c1a4574feac02cd3e22021-11-01T00:00:00Zhttp://aammt.tmmu.edu.cn/Upload/rhtml/202105085.htmhttps://doaj.org/toc/1000-5404 Objective To explore the effect of miRNA-200b on sorafenib resistance in hepatocellular carcinoma cells in order to increase the efficacy of the drug in advanced liver cancer patients. Methods Sorafenib resistant hepatocellular carcinoma HepG2-SR cell line was established by gradually increasing the concentration of sorafenib in the culture medium. The expression of miRNA-200b in HepG2-SR cells, HepG2 cells and miRNA-200b transfected HepG2-SR cells was detected by real-time fluorescence quantitative assay (RT-PCR). In HepG2-SR cells before and after transfection, sorafenib sensitivity was detected by CCK-8 assay, migration and invasion abilities were detected by wound-healing assay and Transwell assay, cell apoptosis was measured by flow cytometry, and expression levels of epithelial mesenchymal transition (EMT) markers were studied by Western blotting. Results Sorafenib resistance was significantly higher and expression of miRNA-200b was significantly lower in HepG2-SR cells than HepG2 cells. Transfection of miRNA-200b mimics resulted in significantly increased miRNA-200b expression, decreased IC50 of sorafenib, reduced cell migration rate and cell invasion, enhanced apoptosis and increased expression of E-cadherin but decreased expression of N-cadherin and Vimentin. Conclusion MiRNA-200b reversed sorafenib resistance of HepG2-SR cells by inducing apoptosis and inhibiting cell proliferation, migration, invasion and EMT.DENG YongTANG TengqianZHANG LeidaEditorial Office of Journal of Third Military Medical Universityarticlehepatocellular carcinomamirna-200bsorafenibdrug resistanceMedicine (General)R5-920ZHDi-san junyi daxue xuebao, Vol 43, Iss 22, Pp 2435-2440 (2021)
institution DOAJ
collection DOAJ
language ZH
topic hepatocellular carcinoma
mirna-200b
sorafenib
drug resistance
Medicine (General)
R5-920
spellingShingle hepatocellular carcinoma
mirna-200b
sorafenib
drug resistance
Medicine (General)
R5-920
DENG Yong
TANG Tengqian
ZHANG Leida
MiRNA-200b reverses drug resistance of hepatocellular carcinoma HepG2 cells to sorafenib and its underlying mechanism
description Objective To explore the effect of miRNA-200b on sorafenib resistance in hepatocellular carcinoma cells in order to increase the efficacy of the drug in advanced liver cancer patients. Methods Sorafenib resistant hepatocellular carcinoma HepG2-SR cell line was established by gradually increasing the concentration of sorafenib in the culture medium. The expression of miRNA-200b in HepG2-SR cells, HepG2 cells and miRNA-200b transfected HepG2-SR cells was detected by real-time fluorescence quantitative assay (RT-PCR). In HepG2-SR cells before and after transfection, sorafenib sensitivity was detected by CCK-8 assay, migration and invasion abilities were detected by wound-healing assay and Transwell assay, cell apoptosis was measured by flow cytometry, and expression levels of epithelial mesenchymal transition (EMT) markers were studied by Western blotting. Results Sorafenib resistance was significantly higher and expression of miRNA-200b was significantly lower in HepG2-SR cells than HepG2 cells. Transfection of miRNA-200b mimics resulted in significantly increased miRNA-200b expression, decreased IC50 of sorafenib, reduced cell migration rate and cell invasion, enhanced apoptosis and increased expression of E-cadherin but decreased expression of N-cadherin and Vimentin. Conclusion MiRNA-200b reversed sorafenib resistance of HepG2-SR cells by inducing apoptosis and inhibiting cell proliferation, migration, invasion and EMT.
format article
author DENG Yong
TANG Tengqian
ZHANG Leida
author_facet DENG Yong
TANG Tengqian
ZHANG Leida
author_sort DENG Yong
title MiRNA-200b reverses drug resistance of hepatocellular carcinoma HepG2 cells to sorafenib and its underlying mechanism
title_short MiRNA-200b reverses drug resistance of hepatocellular carcinoma HepG2 cells to sorafenib and its underlying mechanism
title_full MiRNA-200b reverses drug resistance of hepatocellular carcinoma HepG2 cells to sorafenib and its underlying mechanism
title_fullStr MiRNA-200b reverses drug resistance of hepatocellular carcinoma HepG2 cells to sorafenib and its underlying mechanism
title_full_unstemmed MiRNA-200b reverses drug resistance of hepatocellular carcinoma HepG2 cells to sorafenib and its underlying mechanism
title_sort mirna-200b reverses drug resistance of hepatocellular carcinoma hepg2 cells to sorafenib and its underlying mechanism
publisher Editorial Office of Journal of Third Military Medical University
publishDate 2021
url https://doaj.org/article/ebebf18ffa6548c1a4574feac02cd3e2
work_keys_str_mv AT dengyong mirna200breversesdrugresistanceofhepatocellularcarcinomahepg2cellstosorafenibanditsunderlyingmechanism
AT tangtengqian mirna200breversesdrugresistanceofhepatocellularcarcinomahepg2cellstosorafenibanditsunderlyingmechanism
AT zhangleida mirna200breversesdrugresistanceofhepatocellularcarcinomahepg2cellstosorafenibanditsunderlyingmechanism
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