Phosphatidylinositol 3'-kinase, mTOR, and Glycogen synthase kinase-3β mediated regulation of p21 in human urothelial carcinoma cells
2011

Regulation of p21 in Bladder Cancer Cells

publication Evidence: moderate

Author Information

Author(s): Yohn Nicole L, Bingaman Caitlyn N, DuMont Ashley L, Yoo Lina I

Primary Institution: Department of Biology, Denison University

Hypothesis

How do PI3-kinase and AKT signaling pathways regulate p21 expression in human urothelial carcinoma cells?

Conclusion

The study found that PI3-kinase and AKT signaling lead to increased p21 levels by inhibiting GSK-3β activity and activating mTOR.

Supporting Evidence

  • PI3-kinase and AKT signaling pathways were shown to induce p21 expression.
  • GSK-3β was identified as a negative regulator of p21 levels.
  • Combination treatment with GSK-3β inhibitors and PI3-kinase inhibitors improved cytotoxic effects on bladder cancer cells.

Takeaway

This study shows that certain signals in bladder cancer cells can make a protein called p21 increase, which helps stop the cells from growing too fast.

Methodology

The study used human urothelial carcinoma cell lines and various treatments to analyze the signaling pathways affecting p21 expression.

Limitations

The study primarily used cell lines, which may not fully represent normal urothelial cells.

Statistical Information

P-Value

0.002

Statistical Significance

p<0.05

Digital Object Identifier (DOI)

10.1186/1471-2490-11-19

Want to read the original?

Access the complete publication on the publisher's website

View Original Publication