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Mi-2β promotes immune evasion in melanoma by activating EZH2 methylation

Abstract:
Recent development of new immune checkpoint inhibitors has been particularly successfully in cancer treatment, but still the majority patients fail to benefit. Converting resistant tumors to immunotherapy sensitive will provide a significant improvement in patient outcome. Here we identify Mi-2β as a key melanoma-intrinsic effector regulating the adaptive anti-tumor immune response. Studies in genetically engineered mouse melanoma models indicate that loss of Mi-2β rescues the immune response to immunotherapy in vivo. Mechanistically, ATAC-seq analysis shows that Mi-2β controls the accessibility of IFN-γ-stimulated genes (ISGs). Mi-2β binds to EZH2 and promotes K510 methylation of EZH2, subsequently activating the trimethylation of H3K27 to inhibit the transcription of ISGs. Finally, we develop an Mi-2β-targeted inhibitor, Z36-MP5, which reduces Mi-2β ATPase activity and reactivates ISG transcription. Consequently, Z36-MP5 induces a response to immune checkpoint inhibitors in otherwise resistant melanoma models. Our work provides a potential therapeutic strategy to convert immunotherapy resistant melanomas to sensitive ones.
Publication status:
Published
Peer review status:
Peer reviewed

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Publisher copy:
10.1038/s41467-024-46422-5

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Role:
Author
ORCID:
0000-0003-4995-5521
More by this author
Role:
Author
ORCID:
0000-0002-6451-8787


Publisher:
Springer Nature
Journal:
Nature Communications More from this journal
Volume:
15
Issue:
1
Article number:
2163
Place of publication:
England
Publication date:
2024-03-09
Acceptance date:
2024-02-27
DOI:
EISSN:
2041-1723
Pmid:
38461299


Language:
English
Keywords:
Pubs id:
1788943
Local pid:
pubs:1788943
Deposit date:
2024-03-18
ARK identifier:

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