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- Title
Peroxisome proliferator activated receptor-γ ligands induced cell growth inhibition and its influence on matrix metalloproteinase activity in human myeloid leukemia cells.
- Authors
Jiajun Liu; Huiling Lu; Renwei Huang; Dongjun Lin; Xiangyuan Wu; Qu Lin; Xinyao Wu; Jing Zheng; Xianglin Pan; Jun Peng; Yuqin Song; Maohong Zhang; Ming Hou; Feng Chen
- Abstract
Peroxisome proliferator-activated receptor-gamma (PPAR-γ) is one of the best characterized nuclear hormone receptors (NHRs) in the superfamily of ligand-activated transcriptional factors. PPAR-γ ligands have recently been demonstrated to affect proliferation, differentiation and apoptosis of different cell types. The present study was undertaken to investigate PPAR-γ ligands induced cell growth inhibition and its influence on matrix metalloproteinase MMP-9 and MMP-2 activities on leukemia K562 and HL-60 cells in vitro. The results revealed that PPAR-γ expression was detectable in the two kinds of leukemia cells; Both 15-deoxy-delta(12,14)-prostaglandin J2(15d-PGJ2) and troglitazone (TGZ) have significant growth inhibition effects on these two kinds of leukemia cells. These two PPAR-γ ligands could inhibit the leukemic cell adhesion to the extracellular matrix (ECM) proteins and the invasion through matrigel matrix. The expressions of MMP-9 and MMP-2 as well as their gelatinolytic activities in both HL-60 and K562 cells were inhibited by 15d-PGJ2 and TGZ significantly. We therefore conclude that PPAR-γ ligands 15d-PGJ2 and TGZ have significant growth inhibition effects on myeloid leukemia cells in vitro, and that PPAR-γ ligands can inhibit K562 and HL-60 cell adhesion to and invasion through ECM as well as downregulate MMP-9 and MMP-2 expressions. The data suggest that PPAR-γ ligands may serve as potential anti-leukemia reagents.
- Subjects
ORGANELLE formation; PEROXISOMES; LIGANDS (Biochemistry); CELL growth; METALLOPROTEINASES; MYELOID leukemia; CANCER cells; APOPTOSIS
- Publication
Cancer Chemotherapy & Pharmacology, 2005, Vol 56, Issue 4, p400
- ISSN
0344-5704
- Publication type
Article
- DOI
10.1007/s00280-005-1029-9