CAFs-derived lactate enhances the cancer stemness through inhibiting the MST1 ubiquitination degradation in OSCC
Collectively, our findings suggest that lactic acid from CAFs promotes the CSCs phenotype in OSCC through the DLG5/CUL3/MST1 axis. Therefore, targeting lactic acid exchange between CAFs and tumor cells may provide a novel therapeutic approach to suppress the CSCs phenotype in OSCC.
Authors
- Chuanyu Hu
- Hanzhe Liu (ORCID: https://orcid.org/0000-0001-9001-725X)
- Z. J. Shang (ORCID: https://orcid.org/0000-0002-4884-8129)
- Weilian Liang
- Yang Chen (ORCID: https://orcid.org/0000-0002-1555-1871)
- Jingjing Wang (ORCID: https://orcid.org/0000-0001-5315-5469)
- Yunqing Sun
- Shuzhen Zhang (ORCID: https://orcid.org/0000-0001-7459-3628)
- Ruixue Du
Institutions
- Wuhan University (CN)
- Stomatology Hospital (CN)
- Central Hospital of Wuhan (CN)
- Tongji Hospital (CN)
- Huazhong University of Science and Technology (CN)
- Hubei University (CN)
Publication Details
- Journal
- Cell & Bioscience
- Published
- 2024-11-27
- DOI
- https://doi.org/10.1186/s13578-024-01329-y
- Citations
- 9
- Primary Topic
- Hippo pathway signaling and YAP/TAZ
- Type
- article
- Field-Weighted Citation Impact
- 2.93
Funders
- National Natural Science Foundation of China
- Wuhan University
- Fundamental Research Funds for the Central Universities