TGF-β1/SMAD signaling downregulates KLF4 expression via direct transcriptional suppression and FAT10-mediated proteasomal degradation in hepatocellular carcinoma
Our data suggest that active TGF-β1/SMAD signaling contributes to the loss of KLF4 expression in human HCC through FAT10-mediated ubiquitin-independent proteasomal degradation and direct transcriptional suppression.
Authors
- Senlin Zhao (ORCID: https://orcid.org/0000-0002-6815-2735)
- Zeping Chen (ORCID: https://orcid.org/0009-0002-9879-9211)
- Yichao Lou
- Qi Yao (ORCID: https://orcid.org/0000-0002-9813-4650)
- Hongcheng Sun
- Hanhao Lu
- Desheng Chen
- Jie Lu
Institutions
- Shanghai Medical College of Fudan University (CN)
- Sun Yat-sen University (CN)
- Shanghai Jiao Tong University (CN)
- Wenzhou Medical University (CN)
- Shanghai Chest Hospital (CN)
- Fudan University Shanghai Cancer Center (CN)
- Shanghai First People's Hospital (CN)
- Third Affiliated Hospital of Sun Yat-sen University (CN)
Publication Details
- Journal
- Cell & Bioscience
- Published
- 2026-01-06
- DOI
- https://doi.org/10.1186/s13578-025-01524-5
- Primary Topic
- Kruppel-like factors research
- Type
- article
- Field-Weighted Citation Impact
- 0.00