SIRT6 Deficiency and Its Role in Bladder Cancer
Author Information
Author(s): Wang Xiaojing, Zhang Peipei, Yan Jiaqi, Huang Jingyi, Shen Yan, He Hongchao
Primary Institution: Shanghai Jiao Tong University School of Medicine
Hypothesis
How does SIRT6 deficiency affect glycolysis and lactate secretion in bladder cancer?
Conclusion
SIRT6 deficiency promotes glycolysis and lactate secretion in bladder cancer through the UHRF1/MCT4 axis.
Supporting Evidence
- SIRT6 was down-regulated in bladder cancer and predicts poor overall survival.
- SIRT6 deficiency enhances bladder cancer cell proliferation and migration.
- SIRT6 interacts with UHRF1 and promotes its degradation.
- UHRF1 increases glycolysis via activating MCT4 and HK2 expressions.
- Targeting UHRF1 impairs lactate accumulation in bladder cancer.
Takeaway
When a protein called SIRT6 is missing, bladder cancer cells grow faster and produce more energy in a way that makes them more aggressive.
Methodology
The study used bioinformatic analysis, in vitro and in vivo assays, and measurements of glycolytic abilities.
Limitations
Limited sample size and lack of exploration into the relationship between the SIRT6/UHRF1/MCT4 axis and antitumor immunity.
Statistical Information
P-Value
p<0.05
Statistical Significance
p<0.05
Digital Object Identifier (DOI)
Want to read the original?
Access the complete publication on the publisher's website