KLC3 drives gastric cancer progression by stabilizing SLC2A5 to activate MAPK signaling and promote epithelial-mesenchymal transition
This study identifies KLC3 as a key oncoprotein that promotes GC progression by modulating the MAPK signaling pathway through a novel interaction with the fructose transporter SLC2A5. The KLC3-SLC2A5 axis may serve as a critical link between cellular motor machinery and metabolic reprogramming in cancer, presenting a promising therapeutic target for GC.
Authors
- Xiangjie Li (ORCID: https://orcid.org/0000-0002-9600-8984)
- Zhen Ma (ORCID: https://orcid.org/0000-0001-8650-3714)
- Mali Chen (ORCID: https://orcid.org/0009-0008-2776-8729)
- Hao Chen (ORCID: https://orcid.org/0000-0003-4339-3441)
- Bin Ma (ORCID: https://orcid.org/0000-0002-9030-7393)
- Lin Xiang
- Puyi He
Institutions
- Shanghai Cancer Institute (CN)
- Gansu Provincial Maternal and Child Health Hospital (CN)
- Lanzhou University Second Hospital (CN)
- Lanzhou University (CN)
Publication Details
- Journal
- BMC Cancer
- Published
- 2025-11-11
- DOI
- https://doi.org/10.1186/s12885-025-15084-x
- Citations
- 1
- Primary Topic
- Cancer, Hypoxia, and Metabolism
- Type
- article
- Field-Weighted Citation Impact
- 0.94
Funders
- Lanzhou University