Non-enzymatic SETD1A activity drives breast cancer cell proliferation via cyclin K
SETD1A promotes breast cancer cell replication through its non-enzymatic role via cyclin K, suggesting that the SETD1A-cyclin K axis could be a potential therapeutic target in breast cancer.
Authors
- Bahityar Rahmutulla (ORCID: https://orcid.org/0000-0002-4014-2789)
- Takayuki Hoshii (ORCID: https://orcid.org/0000-0002-5418-1981)
- Masahiko Tanabe (ORCID: https://orcid.org/0000-0002-6558-4399)
- Masaki Fukuyo (ORCID: https://orcid.org/0000-0003-2320-1529)
- Shintaro Izumi
- Atsushi Kaneda (ORCID: https://orcid.org/0000-0002-6980-5515)
- Makoto Matsumoto (ORCID: https://orcid.org/0009-0006-5365-8975)
- Ning Meng (ORCID: https://orcid.org/0000-0002-0481-9916)
- Kanako Hayashi
Institutions
- Chiba University (JP)
- Chiba University Hospital (JP)
- The University of Tokyo (JP)
Publication Details
- Journal
- Breast Cancer Research
- Published
- 2025-08-11
- DOI
- https://doi.org/10.1186/s13058-025-02101-x
- Primary Topic
- Epigenetics and DNA Methylation
- Type
- article
- Field-Weighted Citation Impact
- 0.00
Funders
- Takeda Science Foundation
- Uehara Memorial Foundation
- Japan Agency for Medical Research and Development
- Kobayashi Foundation for Cancer Research
- NOVARTIS Foundation (Japan) for the Promotion of Science
- Japan Society for the Promotion of Science