AUTHOR=Zhang Lin-lin , Li Qi , Zhong Dian-sheng , Zhang Wei-jian , Sun Xiao-jie , Zhu Yu 

TITLE=MCM5 Aggravates the HDAC1-Mediated Malignant Progression of Lung Cancer

JOURNAL=Frontiers in Cell and Developmental Biology

VOLUME=Volume 9 - 2021

YEAR=2021

URL=https://www.frontiersin.org/journals/cell-and-developmental-biology/articles/10.3389/fcell.2021.669132

DOI=10.3389/fcell.2021.669132

ISSN=2296-634X

ABSTRACT=Background: Histone deacetylase 1 (HDAC1) is essential in the malignant progression of tumors. However, not all tumor patients with high HDAC1 expression have poor survival. Herein, we explored the epithelial-to-mesenchymal transition (EMT)-dependent malignant progression of lung cancer caused by the interaction of minichromosome maintenance complex component 5 (MCM5) and HDAC1. Methods: We 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. Results: We 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 metastasis 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. Conclusion: The 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.