MCM5 Aggravates the HDAC1-Mediated Malignant Progression of Lung Cancer
BackgroundHistone deacetylase 1 (HDAC1) is essential in the malignant progression of tumors. However, there is no obvious relationship between the expression of HDAC1 and the survival of lung cancer patients. Herein, we explored the involvement of minichromosome maintenance complex component 5 (MCM5...
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2021-08-01
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doaj-2f30a1cf91ba441f8c0536258b5bb7222021-08-02T15:42:12ZengFrontiers Media S.A.Frontiers in Cell and Developmental Biology2296-634X2021-08-01910.3389/fcell.2021.669132669132MCM5 Aggravates the HDAC1-Mediated Malignant Progression of Lung CancerLin-lin Zhang0Qi Li1Dian-sheng Zhong2Wei-jian Zhang3Xiao-jie Sun4Yu Zhu5Department of Medical Oncology, Tianjin Medical University General Hospital, Tianjin, ChinaDepartment of Pathology, Tianjin Medical University Cancer Institute and Hospital, Tianjin, ChinaDepartment of Medical Oncology, Tianjin Medical University General Hospital, Tianjin, ChinaGraduate School, Tianjin Medical University, Tianjin, ChinaGraduate School, Tianjin Medical University, Tianjin, ChinaDepartment of Clinical Laboratory, Tianjin Haihe Hospital, Tianjin, ChinaBackgroundHistone deacetylase 1 (HDAC1) is essential in the malignant progression of tumors. However, there is no obvious relationship between the expression of HDAC1 and the survival of lung cancer patients. Herein, we explored the involvement of minichromosome maintenance complex component 5 (MCM5) and HDAC1 interaction in the epithelial-to-mesenchymal transition (EMT)-dependent malignant progression of lung cancer.MethodsWe analyzed the expression of MCM5 and HDAC1 in The Cancer Genome Atlas database and clinical samples, as well as their impact on patient survival. Cell and animal experiments were performed to verify the promotion of EMT in lung cancer cells mediated by MCM5 and HDAC1.ResultsWe found that lung adenocarcinoma patients with high expression of MCM5 and HDAC1 had poor survival time. Overexpression of MCM5 and HDAC1 in A549 and H1975 cells can promote proliferation and invasion in vitro and tumor growth and metastasis in vivo. Moreover, astragaloside IV can block the interaction between HDAC1 and MCM5, which can then inhibit the malignant progression of lung cancer in vivo and in vitro.ConclusionThe interaction between MCM5 and HDAC1 aggravated the EMT-dependent malignant progression of lung cancer. Astragaloside IV can block the interaction between MCM5 and HDAC1 to inhibit the progression of lung cancer.https://www.frontiersin.org/articles/10.3389/fcell.2021.669132/fulllung cancerMCM5HDAC1EMTastragaloside IV |
collection |
DOAJ |
language |
English |
format |
Article |
sources |
DOAJ |
author |
Lin-lin Zhang Qi Li Dian-sheng Zhong Wei-jian Zhang Xiao-jie Sun Yu Zhu |
spellingShingle |
Lin-lin Zhang Qi Li Dian-sheng Zhong Wei-jian Zhang Xiao-jie Sun Yu Zhu MCM5 Aggravates the HDAC1-Mediated Malignant Progression of Lung Cancer Frontiers in Cell and Developmental Biology lung cancer MCM5 HDAC1 EMT astragaloside IV |
author_facet |
Lin-lin Zhang Qi Li Dian-sheng Zhong Wei-jian Zhang Xiao-jie Sun Yu Zhu |
author_sort |
Lin-lin Zhang |
title |
MCM5 Aggravates the HDAC1-Mediated Malignant Progression of Lung Cancer |
title_short |
MCM5 Aggravates the HDAC1-Mediated Malignant Progression of Lung Cancer |
title_full |
MCM5 Aggravates the HDAC1-Mediated Malignant Progression of Lung Cancer |
title_fullStr |
MCM5 Aggravates the HDAC1-Mediated Malignant Progression of Lung Cancer |
title_full_unstemmed |
MCM5 Aggravates the HDAC1-Mediated Malignant Progression of Lung Cancer |
title_sort |
mcm5 aggravates the hdac1-mediated malignant progression of lung cancer |
publisher |
Frontiers Media S.A. |
series |
Frontiers in Cell and Developmental Biology |
issn |
2296-634X |
publishDate |
2021-08-01 |
description |
BackgroundHistone deacetylase 1 (HDAC1) is essential in the malignant progression of tumors. However, there is no obvious relationship between the expression of HDAC1 and the survival of lung cancer patients. Herein, we explored the involvement of minichromosome maintenance complex component 5 (MCM5) and HDAC1 interaction in the epithelial-to-mesenchymal transition (EMT)-dependent malignant progression of lung cancer.MethodsWe analyzed the expression of MCM5 and HDAC1 in The Cancer Genome Atlas database and clinical samples, as well as their impact on patient survival. Cell and animal experiments were performed to verify the promotion of EMT in lung cancer cells mediated by MCM5 and HDAC1.ResultsWe found that lung adenocarcinoma patients with high expression of MCM5 and HDAC1 had poor survival time. Overexpression of MCM5 and HDAC1 in A549 and H1975 cells can promote proliferation and invasion in vitro and tumor growth and metastasis in vivo. Moreover, astragaloside IV can block the interaction between HDAC1 and MCM5, which can then inhibit the malignant progression of lung cancer in vivo and in vitro.ConclusionThe interaction between MCM5 and HDAC1 aggravated the EMT-dependent malignant progression of lung cancer. Astragaloside IV can block the interaction between MCM5 and HDAC1 to inhibit the progression of lung cancer. |
topic |
lung cancer MCM5 HDAC1 EMT astragaloside IV |
url |
https://www.frontiersin.org/articles/10.3389/fcell.2021.669132/full |
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