Methyl-Cantharidimide Inhibits Growth of Human Hepatocellular Carcinoma Cells by Inducing Cell Cycle Arrest and Promoting Apoptosis

Methyl-Cantharidimide (MCA) is a derivative of cantharidin which has potential anticancer activity. This study investigates the effect of MCA on the growth and metastasis of human hepatocellular carcinoma (HCC) cells. Human HCC HepG2 and Hep3B2.1-7 cells, and normal hepatocytes (L02) were treated wi...

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Main Authors: Xiangzhong Huang, Wen Xie, Xiaofan Yu, Caiyun Fan, Jin Wang, Yi Cao, Jianxiang Li
Format: Article
Language:English
Published: Frontiers Media S.A. 2019-11-01
Series:Frontiers in Oncology
Subjects:
Online Access:https://www.frontiersin.org/article/10.3389/fonc.2019.01234/full
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spelling doaj-581fc094c1ca4ca6923bbc4c09a5c0532020-11-25T00:46:33ZengFrontiers Media S.A.Frontiers in Oncology2234-943X2019-11-01910.3389/fonc.2019.01234492972Methyl-Cantharidimide Inhibits Growth of Human Hepatocellular Carcinoma Cells by Inducing Cell Cycle Arrest and Promoting ApoptosisXiangzhong Huang0Wen Xie1Xiaofan Yu2Caiyun Fan3Jin Wang4Yi Cao5Jianxiang Li6Department of Interventional Therapy, Affiliated Jiangyin Hospital, Medical College of Southeast University, Jiangyin, ChinaSchool of Public Health, Medical College of Soochow University, Suzhou, ChinaSchool of Public Health, Medical College of Soochow University, Suzhou, ChinaSchool of Public Health, Medical College of Soochow University, Suzhou, ChinaSchool of Public Health, Medical College of Soochow University, Suzhou, ChinaSchool of Public Health, Medical College of Soochow University, Suzhou, ChinaSchool of Public Health, Medical College of Soochow University, Suzhou, ChinaMethyl-Cantharidimide (MCA) is a derivative of cantharidin which has potential anticancer activity. This study investigates the effect of MCA on the growth and metastasis of human hepatocellular carcinoma (HCC) cells. Human HCC HepG2 and Hep3B2.1-7 cells, and normal hepatocytes (L02) were treated with a series of concentrations of MCA. The inhibition ability of these cells was examined by CCK-8 assay. Cell cycle and cell apoptosis were determined using Flow Cytometry. The effect of MCA on cell migration and invasion was evaluated through scratch wound healing and transwell migration assays. Furthermore, Western blot was used to evaluate biomarkers associated with cell cycle and apoptosis. It was found that: (i) MCA inhibited cell proliferation in HCC cells in a dose- and time-dependent manner, especially in HepG2 cells; (ii) MCA arrested HCC cells in G-1 phase cell cycle; (iii) MCA induced HCC cells apoptosis; (iv) MCA inhibited the migration ability of HCC cells; and (v) MCA treatment significantly increased cleaved-caspase3 and decreased NF-κB protein in HCC cells. These results suggest that MCA has cytotoxic effect on HCC cells by inducing cell cycle arrest and promoting apoptosis. MCA could be developed as an previous anticancer drug for the treatment of human hepatocellular carcinoma.https://www.frontiersin.org/article/10.3389/fonc.2019.01234/fullmethyl-cantharidimide (MCA)cantharidin (CTD)hepatocellular carcinomacell growthinvasion
collection DOAJ
language English
format Article
sources DOAJ
author Xiangzhong Huang
Wen Xie
Xiaofan Yu
Caiyun Fan
Jin Wang
Yi Cao
Jianxiang Li
spellingShingle Xiangzhong Huang
Wen Xie
Xiaofan Yu
Caiyun Fan
Jin Wang
Yi Cao
Jianxiang Li
Methyl-Cantharidimide Inhibits Growth of Human Hepatocellular Carcinoma Cells by Inducing Cell Cycle Arrest and Promoting Apoptosis
Frontiers in Oncology
methyl-cantharidimide (MCA)
cantharidin (CTD)
hepatocellular carcinoma
cell growth
invasion
author_facet Xiangzhong Huang
Wen Xie
Xiaofan Yu
Caiyun Fan
Jin Wang
Yi Cao
Jianxiang Li
author_sort Xiangzhong Huang
title Methyl-Cantharidimide Inhibits Growth of Human Hepatocellular Carcinoma Cells by Inducing Cell Cycle Arrest and Promoting Apoptosis
title_short Methyl-Cantharidimide Inhibits Growth of Human Hepatocellular Carcinoma Cells by Inducing Cell Cycle Arrest and Promoting Apoptosis
title_full Methyl-Cantharidimide Inhibits Growth of Human Hepatocellular Carcinoma Cells by Inducing Cell Cycle Arrest and Promoting Apoptosis
title_fullStr Methyl-Cantharidimide Inhibits Growth of Human Hepatocellular Carcinoma Cells by Inducing Cell Cycle Arrest and Promoting Apoptosis
title_full_unstemmed Methyl-Cantharidimide Inhibits Growth of Human Hepatocellular Carcinoma Cells by Inducing Cell Cycle Arrest and Promoting Apoptosis
title_sort methyl-cantharidimide inhibits growth of human hepatocellular carcinoma cells by inducing cell cycle arrest and promoting apoptosis
publisher Frontiers Media S.A.
series Frontiers in Oncology
issn 2234-943X
publishDate 2019-11-01
description Methyl-Cantharidimide (MCA) is a derivative of cantharidin which has potential anticancer activity. This study investigates the effect of MCA on the growth and metastasis of human hepatocellular carcinoma (HCC) cells. Human HCC HepG2 and Hep3B2.1-7 cells, and normal hepatocytes (L02) were treated with a series of concentrations of MCA. The inhibition ability of these cells was examined by CCK-8 assay. Cell cycle and cell apoptosis were determined using Flow Cytometry. The effect of MCA on cell migration and invasion was evaluated through scratch wound healing and transwell migration assays. Furthermore, Western blot was used to evaluate biomarkers associated with cell cycle and apoptosis. It was found that: (i) MCA inhibited cell proliferation in HCC cells in a dose- and time-dependent manner, especially in HepG2 cells; (ii) MCA arrested HCC cells in G-1 phase cell cycle; (iii) MCA induced HCC cells apoptosis; (iv) MCA inhibited the migration ability of HCC cells; and (v) MCA treatment significantly increased cleaved-caspase3 and decreased NF-κB protein in HCC cells. These results suggest that MCA has cytotoxic effect on HCC cells by inducing cell cycle arrest and promoting apoptosis. MCA could be developed as an previous anticancer drug for the treatment of human hepatocellular carcinoma.
topic methyl-cantharidimide (MCA)
cantharidin (CTD)
hepatocellular carcinoma
cell growth
invasion
url https://www.frontiersin.org/article/10.3389/fonc.2019.01234/full
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