Possible mechanisms underlying acceleration of proliferation by 15-deoxy-.DELTA.12,14-prostaglandin J2 and the precursors in human T acute lymphoblastic leukemia cell line CCRF-CEM.
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15-Deoxy-Δ<SUP>12, 14</SUP>-prostaglandin J<SUB>2</SUB> (15dPGJ<SUB>2</SUB> ), that is a ligand for peroxisome proliferator-activated receptor γ (PPAR γ), induced apoptosis of human several tumors including gastric, lung, colon, prostate and breast. However, the role of PPAR y signals in other types of cancer cells such as leukemia except solid cancer cells is still unclear. The aim of this study is to evaluate the ability of 15dPGJ<SUB>2</SUB> on the proliferation of human T acute lymphoblastic leukemia cell line CCRF-CEM. 15dPGJ<SUB>2</SUB> at 5 M stimulated the proliferation in CCRF-CEM at 1 to 3 days after incubation. In contrast, 15dPGJ<SUB>2</SUB> at concentrations of above 10 M inhibited the proliferation. PGD<SUB>2</SUB>, PGJ<SUB>2</SUB> and Δ<SUP>12</SUP>PGJ<SUB>2</SUB> (ΔPGJ<SUB>2</SUB>), those are precursors of 15dPGJ<SUB>2</SUB>, had similarly proliferative effects, whereas they showed anti-proliferative effects at high concentrations. Both SB203580, a p38 mitogen-activated protein kinase ( MAPK ) inhibitor, and LY294002, a phosphoinositide 3-kinase ( PI3K) inhibitor, prevented 15dPGJ<SUB>2</SUB> and three precursors-accelerated proliferation in CCRF-CEM. In contrast, PD98059, an extracellular signal-related kinase 1/2 inhibitor, did not affect 15dPGJ<SUB>2</SUB> and three precursors-accelerated proliferation. Immunoblotting analysis revealed that PGD<SUB>2</SUB> at 5 μM, PGJ<SUB>2</SUB> at 5 μM, ΔPGJ<SUB>2</SUB> at 1μ M and 15dPGJ<SUB>2</SUB> at 5 μM potentiated the expression of cyclin A, without affecting the expression of Cdk inhibitors including p18, p21, p27 in CCRF-CEM. These results suggest that PGD<SUB>2</SUB>, PGJ<SUB>2</SUB>, ΔPGJ<SUB>2</SUB> and 15dPGJ<SUB>2</SUB> may, through the activation of p38 MAPK and/or PI3K, potentiate the expression of cyclin A, leading to acceleration of proliferation in CCRF-CEM.
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