Aberrantly expressed HORMAD1 disrupts nuclear localization of MCM8–MCM9 complex and compromises DNA mismatch repair in cancer cells

HORMAD1 is a meiosis-specific protein that promotes synapsis and recombination of homologous chromosomes in meiotic prophase. Originally identified as a cancer/testis antigen, HORMAD1 is also aberrantly expressed in several cancers. However, the functions of HORMAD1 in cancer cells are still not cle...

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Published in:Cell death & disease 2020-07, Vol.11 (7), p.519-519, Article 519
Main Authors: Liu, Kang, Wang, Yifan, Zhu, Quanfeng, Li, Peng, Chen, Jiyuan, Tang, Zhenghui, Shen, Yuanming, Cheng, Xiaodong, Lu, Lin-Yu, Liu, Yidan
Format: Article
Language:English
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631/337/1427/2121
631/67/68
82/29
82/80
Animals
Antibodies
Biochemistry
Biomedical and Life Sciences
Cancer
Cell Biology
Cell Culture
Cell Cycle Proteins - metabolism
Chromatin
Chromosomes
Deoxyribonucleic acid
DNA
DNA Mismatch Repair - genetics
DNA repair
Female
Genomic instability
Homologous recombination
Humans
Immunology
Life Sciences
Localization
Male
Meiosis
Mice
Mice, Knockout
Minichromosome Maintenance Proteins - genetics
Mismatch repair
MLH1 protein
Neoplasms - genetics
Prophase
Yeast
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Liu, Yidan
description HORMAD1 is a meiosis-specific protein that promotes synapsis and recombination of homologous chromosomes in meiotic prophase. Originally identified as a cancer/testis antigen, HORMAD1 is also aberrantly expressed in several cancers. However, the functions of HORMAD1 in cancer cells are still not clear. Here, we show that HORMAD1 is aberrantly expressed in a wide variety of cancers and compromises DNA mismatch repair in cancer cells. Mechanistically, HORMAD1 interacts with MCM8–MCM9 complex and prevents its efficient nuclear localization. As a consequence, HORMAD1-expressing cancer cells have reduced MLH1 chromatin binding and DNA mismatch repair defects. Consistently, HORMAD1 expression is associated with increased mutation load and genomic instability in many cancers. Taken together, our study provides mechanistic insights into HORMAD1’s functions in cancer cells, which can potentially be exploited for targeted therapy of HORMAD1-expressing cancers.
doi_str_mv 10.1038/s41419-020-2736-1
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subjects 631/337/1427/2121
631/67/68
82/29
82/80
Animals
Antibodies
Biochemistry
Biomedical and Life Sciences
Cancer
Cell Biology
Cell Culture
Cell Cycle Proteins - metabolism
Chromatin
Chromosomes
Deoxyribonucleic acid
DNA
DNA Mismatch Repair - genetics
DNA repair
Female
Genomic instability
Homologous recombination
Humans
Immunology
Life Sciences
Localization
Male
Meiosis
Mice
Mice, Knockout
Minichromosome Maintenance Proteins - genetics
Mismatch repair
MLH1 protein
Neoplasms - genetics
Prophase
Yeast
title Aberrantly expressed HORMAD1 disrupts nuclear localization of MCM8–MCM9 complex and compromises DNA mismatch repair in cancer cells
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