Phase-separating fusion proteins drive cancer by upsetting transcription regulation
We find that proteins initiating LLPS are frequently implicated in somatic cancers, even surpassing their involvement in neurodegeneration. Our data shows that cancer-driving LLPS scaffolds tend to be potent oncogenes, giving rise to dominant phenotypes and lacking targeting options by current FDA-approved drugs. Finding the currently missing drugs to shut down oncogenic fusion proteins, to disrupt the condensation enabled by them, and to offset their downstream effects could provide cancer drugs widely applicable to diverse cancer incidences previously defying standard treatments.
Authors
- Péter Tompa (ORCID: https://orcid.org/0000-0001-8042-9939)
- Tamás Lázár (ORCID: https://orcid.org/0000-0001-7496-6711)
- Bálint Mészáros (ORCID: https://orcid.org/0000-0003-0919-4449)
- Rita Pancsa (ORCID: https://orcid.org/0000-0003-0849-9312)
- Nazanin Farahi (ORCID: https://orcid.org/0000-0002-6834-8578)
Institutions
- St. Jude Children's Research Hospital (US)
- Vrije Universiteit Brussel (BE)
- Vlaams Instituut voor Biotechnologie (BE)
- National Institute of Oncology (HU)
- VIB-VUB Center for Structural Biology (BE)
- European Molecular Biology Laboratory (DE)
- HUN-REN Research Centre for Natural Sciences (HU)
Publication Details
- Journal
- Genome biology
- Published
- 2025-10-02
- DOI
- https://doi.org/10.1186/s13059-025-03787-0
- Citations
- 2
- Primary Topic
- RNA Research and Splicing
- Type
- article
- Field-Weighted Citation Impact
- 1.61