The Antiproliferative Effects Of Melatonin On Experimental Pituitary And Colonic Tumors

Possible Involvement ofthe Putative Nuclear Binding Site?

Marek Pawlikowski, Jolanta Kunert-Radek, Katarzyna Winczyk, Gabriela Melen-Mucha, Anna Gruszka, and Michal Karasek*

Institute of Endocrinology and * Laboratory of Electron Microscopy Chair of Pathomorphology Medical University of Lodz 91-425 Lodz, Poland

1. INTRODUCTION

It has been repeatedly shown that the pineal hormone melatonin (MLT) inhibits the growth of various experimental tumors in rodents. The oncostatic action of MLT is connected, at least in part, with its antiproliferative effects on the tumor cells. However, the molecular mechanisms by which MLT suppresses cell proliferation still remains unclear. It was suggested that MLT acts not only via membrane receptors but also via nuclear binding sites and the latter are identical with so-called RZR/ROR a-receptors (2,6). Since a synthetic thiazolidinedione compound CGP 52608 has been recently shown to be an exogenous ligand for RZR/ROR receptors it seemed to us worthwhile to see whether it exerts also the antiproliferative effects. We have studied the effects of MLT and CGP 52608 on cell proliferation of the diethylstilbestrol (DES)-induced rat pituitary tumors and of the murine colonic adenocarcinoma Colon 38.

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