Article
An exogenous cdk inhibitor, butyrolactone-I, induces apoptosis with increased Bax/Bcl-2 ratio in p53-mutated pancreatic cancer cells.
Anticancer research - 1 Jan 2000
Wada M, Hosotani R, Lee J U, Doi R, Koshiba T, Fujimoto K, Miyamoto Y, Tsuji S, Nakajima S, Okuyama A, Imamura M
Abstract excerpt
We investigated the effects of an exogenous cdk inhibitor, butyrolactone-I, on cell growth inhibition, apoptosis induction, and the regulation of apoptosis in pancreatic cancer cells with mutated p53. Cell growth was dose-dependently inhibited by Butyrolactone-I in PANC-1 and AsPC-1 cells. Phosph...
Topics
- 4-Butyrolactone
- Apoptosis
- Cell Survival
- Cyclin A
- Cyclin-Dependent Kinases
- Enzyme Inhibitors
- Genes, bcl-2
- Genes, p53
- Humans
- Kinetics
- Mutation
- Pancreatic Neoplasms
- Phosphorylation
- Proto-Oncogene Proteins
- Proto-Oncogene Proteins c-bcl-2