Abstract
The growth of human cancer cells expressing peroxisome proliferator-activated receptor-γ (PPAR-γ) has been reported to be inhibited by PPAR-γ ligands. In esophageal squamous-cell carcinoma cell lines T.T, T.Tn, and EC-GI-10, we detected expression of PPAR-γ and investigated the effects of PPAR-γ ligands on these cell lines in vitro with the use of troglitazone, pioglitazone, and 15d-PGJ2. Marked growth inhibition by the PPAR-γ ligands was observed in all cases. The growth-inhibitory effect was evidenced by a dose-dependent inhibition of deoxyribonucleic acid synthesis and was associated with altered cell-cycle progression manifesting G1 arrest. Cell-cycle arrest in T.Tn cells induced by troglitazone could be correlated with an increased level of cyclin-dependent kinase inhibitor p27Kip1, p21Cip1/Waf1, and p18Ink4c. Moreover, troglitazone treatment increased the expression of interleukin-1α, a multifunctional cytokine implicated in antitumor immunity. These findings suggest that troglitazone and other PPAR-γ ligands have adjuvant or neoadjuvant therapeutic potentials in esophageal cancer. (J Lab Clin Med 2002;140:17-26)
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