RESUMO
Purpose:To investigate palitaxel (Tax) induct io n of apoptosis in human retinoblastoma Y79 cells and the role of Bcl-2 phosphor ylation in the mechanism. Methods:Antiproliferation effects of Tax on Y79 cells were dete rmined by 3H-thymidine incorporation. Apoptosis of the Tax-treated cells was determined by DNA fragmentation analysis. Bcl-2 phosphorylation was determ ined by Western blot analysis. Cell transfection was used in mutant Bcl-2 trans fecting in Y79 cells. Results:After 24 hours treatment with 1 ?mol/L Tax, 3H- thymidine incorporation decreased in Y79 cells and the effects were time and dos e dependent. DNA ladder appeared in DNA fragmantation analysis after 12-24 hour s treatment with Tax. Bcl-2 Phosphorylation was significantly increased in 12- 24 hours treatment with Tax. Bcl-2, a mutant of Bcl-2, blocked Tax activation process. Conclusions:Tax inhibits cell growth and induces apoptosis in h uman Y79 cells, and phosphorylation of Bcl-2 might be involved in this process.
RESUMO
Objective: To investigate all trans retinoid Acid (ATRA) inhibition of cell growth in human retinoblastoma Y79 cells, and its mechanism. Methods: Antiproliferation effects of ATRA on Y79 cells were determined by 3 H thymidine incorporation. Cell cycle analysis was performed by flow cytometry. JNK phosphorylation was analyzed by Western blot analysis. Results: After 36 h treatment with 10 -6 mol?L -1 ATRA, 3 H thymidine incorporation decreased to 40%, under the same condition, Y79 cells were arrested in G 0 /G 1 and Sub G 1 peak appeared. Curcumin, JNK blocker, blocked the growth inhibition by ATRA. JNK was phosphorylated in 10 to 20 min. Conclusion: JNK phosphorylating mediated ATRA inhibition of apoptosis in Y79 cells. These results suggested that ATRA might have clinical application for treatment of retinoblastoma.