YTHDF2 promotes anaplastic thyroid cancer progression by activating the DDIT4/AKT/mTOR signaling pathway
This study is the first to demonstrate that elevated YTHDF2 expression levels suppress DDIT4 expression in an m6A-dependent manner and activate the AKT/mTOR signaling pathway, thereby promoting ATC progression. YTHDF2 plays a pivotal role in ATC progression, and it may serve as a promising therapeutic target in the future.
Authors
- Lingyun Zhang (ORCID: https://orcid.org/0000-0002-3471-2634)
- Muye Song
- Shikuo Rong (ORCID: https://orcid.org/0000-0001-7904-0096)
- Lei Xu (ORCID: https://orcid.org/0000-0002-1862-786X)
- Zeyu Wu (ORCID: https://orcid.org/0000-0002-1104-0839)
- Linhe Wang (ORCID: https://orcid.org/0000-0001-7365-5209)
- Ziteng Lan
- Jian Chen (ORCID: https://orcid.org/0000-0001-7535-6499)
- Jinghua Li (ORCID: https://orcid.org/0000-0002-1805-9970)
- Weijian Chen (ORCID: https://orcid.org/0000-0003-2154-5619)
- Yongchen Liu (ORCID: https://orcid.org/0000-0002-1772-5572)
- Bao Dai
Institutions
- Jinan University (CN)
- Southern University of Science and Technology (CN)
- Guangdong Academy of Medical Sciences (CN)
- Guangdong Provincial People's Hospital (CN)
- Southern Medical University (CN)
Publication Details
- Journal
- Biology Direct
- Published
- 2024-11-26
- DOI
- https://doi.org/10.1186/s13062-024-00566-y
- Citations
- 8
- Primary Topic
- RNA modifications and cancer
- Type
- article
- Field-Weighted Citation Impact
- 1.87
Funders
- Natural Science Foundation of Guangdong Province