Histone N-terminal acetyltransferase NAA40 links one-carbon metabolism to chemoresistance

被引:0
|
作者
Christina Demetriadou
Anastasia Raoukka
Evelina Charidemou
Constantine Mylonas
Christina Michael
Swati Parekh
Costas Koufaris
Paris Skourides
Panagiotis Papageorgis
Peter Tessarz
Antonis Kirmizis
机构
[1] University of Cyprus,Department of Biological Sciences
[2] Max Planck Institute for Biology of Ageing,Department of Life Sciences
[3] European University Cyprus,undefined
[4] Cologne Excellence Cluster on Stress Responses in ageing-associated Diseases (CECAD),undefined
来源
Oncogene | 2022年 / 41卷
关键词
D O I
暂无
中图分类号
学科分类号
摘要
Aberrant function of epigenetic modifiers plays an important role not only in the progression of cancer but also the development of drug resistance. N-alpha-acetyltransferase 40 (NAA40) is a highly specific epigenetic enzyme catalyzing the transfer of an acetyl moiety at the N-terminal end of histones H4 and H2A. Recent studies have illustrated the essential oncogenic role of NAA40 in various cancer types but its role in chemoresistance remains unclear. Here, using transcriptomic followed by metabolomic analysis in colorectal cancer (CRC) cells, we demonstrate that NAA40 controls key one-carbon metabolic genes and corresponding metabolites. In particular, through its acetyltransferase activity NAA40 regulates the methionine cycle thereby affecting global histone methylation and CRC cell survival. Importantly, NAA40-mediated metabolic rewiring promotes resistance of CRC cells to antimetabolite chemotherapy in vitro and in xenograft models. Specifically, NAA40 stimulates transcription of the one-carbon metabolic gene thymidylate synthase (TYMS), whose product is targeted by 5-fluorouracil (5-FU) and accordingly in primary CRC tumours NAA40 expression associates with TYMS levels and poorer 5-FU response. Mechanistically, NAA40 activates TYMS by preventing enrichment of repressive H2A/H4S1ph at the nuclear periphery. Overall, these findings define a novel regulatory link between epigenetics and cellular metabolism mediated by NAA40, which is harnessed by cancer cells to evade chemotherapy.
引用
收藏
页码:571 / 585
页数:14
相关论文
共 50 条
  • [31] Structural determinants and cellular environment define processed actin as the sole substrate of the N-terminal acetyltransferase NAA80
    Goris, Marianne
    Magin, Robert S.
    Foyn, Havard
    Myklebust, Line M.
    Varland, Sylvia
    Ree, Rasmus
    Drazic, Adrian
    Bhambra, Parminder
    Stove, Svein I.
    Baumann, Markus
    Haug, Bengt Erik
    Marmorstein, Ronen
    Arnesen, Thomas
    PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2018, 115 (17) : 4405 - 4410
  • [32] Proximal partners of the organellar N-terminal acetyltransferase NAA60: insights into Golgi structure and transmembrane protein topology
    Tanco, Sebastian
    Jonckheere, Veronique
    Tharkeshwar, Arun Kumar
    Bogaert, Annelies
    Gevaert, Kris
    Anneart, Wim
    Van Damme, Petra
    OPEN BIOLOGY, 2025, 15 (02)
  • [33] Uteroplacental insufficiency alters DNA methylation, one-carbon metabolism, and histone acetylation in IUGR rats
    MacLennan, NK
    James, SJ
    Melnyk, S
    Piroozi, A
    Jernigan, S
    Hsu, JL
    Janke, SM
    Pham, TD
    Lane, RH
    PHYSIOLOGICAL GENOMICS, 2004, 18 (01) : 43 - 50
  • [34] One-carbon metabolism supports S-Adenosylmethionine and histone methylation to drive inflammatory macrophages
    Yu, W.
    Wang, Z.
    Zhang, K.
    Wang, D.
    EUROPEAN JOURNAL OF IMMUNOLOGY, 2019, 49 : 1280 - 1281
  • [35] One-Carbon Metabolism Supports S-Adenosylmethionine and Histone Methylation to Drive Inflammatory Macrophages
    Yu, Weiwei
    Wang, Zhen
    Zhang, Kailian
    Chi, Zhexu
    Xu, Ting
    Jiang, Danlu
    Chen, Sheng
    Li, Wenxin
    Yang, Xuyan
    Zhang, Xue
    Wu, Yingliang
    Wang, Di
    MOLECULAR CELL, 2019, 75 (06) : 1147 - +
  • [36] NAA10 mutation causing a novel intellectual disability syndrome with Long QT due to N-terminal acetyltransferase impairment
    Jillian P. Casey
    Svein I. Støve
    Catherine McGorrian
    Joseph Galvin
    Marina Blenski
    Aimee Dunne
    Sean Ennis
    Francesca Brett
    Mary D. King
    Thomas Arnesen
    Sally Ann Lynch
    Scientific Reports, 5
  • [37] NAA10p.(N101K) disrupts N-terminal acetyltransferase complex NatA and is associated with developmental delay and hemihypertrophy
    McTiernan, Nina
    Gill, Harinder
    Prada, Carlos E.
    Pachajoa, Harry
    Lores, Juliana
    Arnesen, Thomas
    EUROPEAN JOURNAL OF HUMAN GENETICS, 2021, 29 (02) : 280 - 288
  • [38] Folate enzyme MTHFD2 links one-carbon metabolism to unfolded protein response in glioblastoma
    Zhu, Zhiyuan
    Kiang, Karrie Mei-Yee
    Li, Ning
    Liu, Jiaxin
    Zhang, Pingde
    Jin, Lei
    He, Xiaozheng
    Zhang, Shizhong
    Leung, Gilberto Ka-Kit
    CANCER LETTERS, 2022, 549
  • [39] NAA10 p.(N101K) disrupts N-terminal acetyltransferase complex NatA and is associated with developmental delay and hemihypertrophy
    Nina McTiernan
    Harinder Gill
    Carlos E. Prada
    Harry Pachajoa
    Juliana Lores
    Thomas Arnesen
    European Journal of Human Genetics, 2021, 29 : 280 - 288
  • [40] Recruitment of histone acetyltransferase activity by the N-terminal homology domain of Pygopus augments TCF-dependent transcriptional activation
    Andrews, Phillip
    Kao, Kenneth
    Popadiuk, Catherine
    CANCER RESEARCH, 2009, 69