Rapamycin-induced apoptosis is p53-independent in human prostate carcinoma PC-3 cells
- C Ahn
- M Hwang
- P Ramsamooj
- S Lee
- M Jung
Affiliations: GEORGETOWN UNIV,DEPT RADIAT MED,WASHINGTON,DC 20007. US FDA,DIV ONCOL,ROCKVILLE,MD 20857. US FDA,DIV DRUG PROD & RES & TESTING,ROCKVILLE,MD 20857.
- Published online on: November 1, 1997 https://doi.org/10.3892/ijo.11.5.1115
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We have investigated the mechanisms of rapamycin-induced growth inhibition and apoptosis in the PC-3 prostate carcinoma cell line. Rapamycin induced apoptosis as well as the expression of p21(waf1) mRNA and protein, independent of p53. Rapamycin treatment also resulted in: a decrease in cdk2 kinase activity; an increase in hypophosphorylated retinoblastoma protein (pRb); a dephosphorylation of p70 S6 kinase; and, growth-arrest in G(1)-phase of cell cycle. These data suggest that rapamycin-induced growth arrest and apoptosis occur through the p53-independent induction of p21(waf1). Since this induction occurred soon after rapamycin treatment, possibly, the early induction of p21(waf1) and G(1)-arrest are important components of the mechanism by which rapamycin induces apoptosis in PC-3 cells.