Impaired histone inheritance promotes tumor progression

Congcong Tian, Jiaqi Zhou, Xinran Li, Yuan Gao, Qing Wen, Xing Kang, Nan Wang, Yuan Yao, Jiuhang Jiang, Guibing Song, Tianjun Zhang, Suili Hu, JingYi Liao, Chuanhe Yu, Zhiquan Wang, Xiangyu Liu, Xinhai Pei, Kuiming Chan, Zichuan Liu and Haiyun Gan ()
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Congcong Tian: Chinese Academy of Sciences
Jiaqi Zhou: Chinese Academy of Sciences
Xinran Li: Chinese Academy of Sciences
Yuan Gao: Cold Spring Harbor Laboratory
Qing Wen: Chinese Academy of Sciences
Xing Kang: Chinese Academy of Sciences
Nan Wang: Chinese Academy of Sciences
Yuan Yao: Chinese Academy of Sciences
Jiuhang Jiang: Chinese Academy of Sciences
Guibing Song: Chinese Academy of Sciences
Tianjun Zhang: Chinese Academy of Sciences
Suili Hu: Chinese Academy of Sciences
JingYi Liao: Chinese Academy of Sciences
Chuanhe Yu: University of Minnesota
Zhiquan Wang: Mayo Clinic
Xiangyu Liu: Shenzhen University Health Science Center
Xinhai Pei: Shenzhen University Health Science Center
Kuiming Chan: City University of Hong Kong
Zichuan Liu: Tianjin University
Haiyun Gan: Chinese Academy of Sciences

Nature Communications, 2023, vol. 14, issue 1, 1-17

Abstract: Abstract Faithful inheritance of parental histones is essential to maintain epigenetic information and cellular identity during cell division. Parental histones are evenly deposited onto the replicating DNA of sister chromatids in a process dependent on the MCM2 subunit of DNA helicase. However, the impact of aberrant parental histone partition on human disease such as cancer is largely unknown. In this study, we construct a model of impaired histone inheritance by introducing MCM2-2A mutation (defective in parental histone binding) in MCF-7 breast cancer cells. The resulting impaired histone inheritance reprograms the histone modification landscapes of progeny cells, especially the repressive histone mark H3K27me3. Lower H3K27me3 levels derepress the expression of genes associated with development, cell proliferation, and epithelial to mesenchymal transition. These epigenetic changes confer fitness advantages to some newly emerged subclones and consequently promote tumor growth and metastasis after orthotopic implantation. In summary, our results indicate that impaired inheritance of parental histones can drive tumor progression.

Date: 2023
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DOI: 10.1038/s41467-023-39185-y

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