SUMO3 inhibition by butyric acid suppresses cell viability and glycolysis and promotes gemcitabine antitumor activity in pancreatic cancer
SUMO3 acted as an active molecule in cell survival and growth by enhancing glycolysis in response to either GEM or BA. The mechanism was related to the constitutive IκBα/NF-κB/SUMO3/β-catenin signaling pathway.
Authors
- Changjing Huang
- Liming Zhu (ORCID: https://orcid.org/0000-0001-5839-3765)
- Gang Chen (ORCID: https://orcid.org/0000-0002-4864-1451)
- Huifeng Gao
- Yehua Shen
- Yilin Wang (ORCID: https://orcid.org/0009-0003-7583-4704)
Institutions
- Nanjing University of Chinese Medicine (CN)
- Shanghai Medical College of Fudan University (CN)
- Fudan University Shanghai Cancer Center (CN)
- Wuxi Taihu Hospital (CN)
- Wuxi People's Hospital (CN)
- Children's Hospital of Fudan University (CN)
Publication Details
- Journal
- Biology Direct
- Published
- 2024-08-26
- DOI
- https://doi.org/10.1186/s13062-024-00513-x
- Citations
- 7
- Primary Topic
- Ubiquitin and proteasome pathways
- Type
- article
- Field-Weighted Citation Impact
- 1.64
Funders
- National Natural Science Foundation of China