Abstract:
:The mechanisms underlying how cells subjected to genotoxic stress reestablish reduction-oxidation (redox) homeostasis to scavenge genotoxic stress-induced reactive oxygen species (ROS), which maintains the physiological function of cellular processes and cell survival, remain unclear. Herein, we report that, via a TCF-independent mechanism, genotoxic stress induces the enrichment of β-catenin in chromatin, where it forms a complex with ATM phosphorylated-JDP2 and PRMT5. This elicits histone H3R2me1/H3R2me2s-induced transcriptional activation by the recruitment of the WDR5/MLL methyltransferase complexes and concomitant H3K4 methylation at the promoters of multiple genes in GSH-metabolic cascade. Treatment with OICR-9429, a small-molecule antagonist of the WDR5-MLL interaction, inhibits the β-catenin/JDP2/PRMT5 complex-reestablished GSH metabolism, leading to a lethal increase in the already-elevated levels of ROS in the genotoxic-agent treated cancer cells. Therefore, our results unveil a plausible role for β-catenin in reestablishing redox homeostasis upon genotoxic stress and shed light on the mechanisms of inducible chemotherapy resistance in cancer.
journal_name
Nat Communjournal_title
Nature communicationsauthors
Cao L,Wu G,Zhu J,Tan Z,Shi D,Wu X,Tang M,Li Z,Hu Y,Zhang S,Yu R,Mo S,Wu J,Song E,Li M,Song L,Li Jdoi
10.1038/s41467-019-11696-7subject
Has Abstractpub_date
2019-08-21 00:00:00pages
3761issue
1issn
2041-1723pii
10.1038/s41467-019-11696-7journal_volume
10pub_type
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