Inhibition of BRD4 attenuated IFNγ-induced apoptosis in colorectal cancer organoids
Our results showed that the inhibition of Brd4 suppressed IFNγ-induced cytotoxicity by modulating the Jak-Stat pathway. These data suggested that the inhibition of Brd4 could increase cell viability in the cancer microenvironment where IFNγ is abundant, revealing a new aspect of the molecular mechanism of CRC development. Our results may help in evaluating the application of Bet inhibitors in treating CRC. Additionally, our RNA-seq data sets will be helpful for clarifying the relationship between Brd4 and immunomodulators, such as Il33, or for studying the responses of colonic epithelial cells to IFNγ.
Authors
- Akimi Yonezawa
- Koji Okamoto (ORCID: https://orcid.org/0000-0001-7587-0164)
- Haruna Takeda (ORCID: https://orcid.org/0000-0002-1643-2524)
- Kana Shimomura
Institutions
- National Cancer Research Institute (GB)
- Teikyo University (JP)
Publication Details
- Journal
- BMC Cancer
- Published
- 2025-01-23
- DOI
- https://doi.org/10.1186/s12885-025-13544-y
- Citations
- 1
- Primary Topic
- Protein Degradation and Inhibitors
- Type
- article
- Field-Weighted Citation Impact
- 0.81
Funders
- Japan Agency for Medical Research and Development
- Japan Society for the Promotion of Science
- Japan Science and Technology Agency