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Growth-inhibitory activity of melatonin on human androgen-independent DU 145 prostate cancer cells
M M Marelli1, P Limonta, R Maggi
1Center for Endocrinological Oncology, University of Milan, Milan, Italy.
Background:
The pineal hormone melatonin has been shown to exert a direct oncostatic activity on neoplastic cells, particularly from breast cancer. In the present study, we evaluated the effects of melatonin on the proliferation and on the cell cycle distribution of human androgen-independent DU 145 prostate cancer cells. Experiments were also performed to gain insights into the possible mechanism of action of the hormone.
Methods:
The effects of melatonin on DU 145 cell proliferation was analyzed by counting the cells by hemocytometer at the end of treatment. The effects of the pineal hormone on cell cycle distribution were evaluated by FACS analysis. RT-PCR studies were performed to detect Mel(1a) and Mel(1b) expression in DU 145 cells. The cellular localization of (125)I-melatonin binding sites was investigated by radioreceptor assay. A commercially available binding-protein assay kit was utilized to evaluate intracellular cAMP levels.
Results:
Melatonin, in physiological doses, significantly inhibited DU 145 cell proliferation and induced cell cycle withdrawal by accumulating cells in G0/G1 phase. The mRNA for Mel(1a) receptors was found to be expressed in DU 145 cells; however, by radioreceptor assay, no binding sites for (125)I-melatonin could be detected in membrane preparations, suggesting that, in these cells, the level of translation of this mRNA is too low to possibly mediate the antiproliferative action of the hormone. In agreement with this hypothesis, melatonin did not affect forskolin-induced intracellular cAMP accumulation. Binding sites for (125)I-melatonin were found in nuclear extracts of DU 145 cells.
Conclusions:
Melatonin exerts a direct oncostatic activity on human androgen-independent prostate cancer cells, by affecting cell cycle progression. This activity seems to be mediated by nuclear, but not by membrane, receptors.
Insights
Melatonin, a pineal hormone, inhibits prostate cancer cell growth by halting cell cycle progression. This oncostatic effect on androgen-independent DU 145 cells appears to be mediated by nuclear receptors.
Area of Science:
- Oncology
- Endocrinology
- Cell Biology
Background:
- Melatonin exhibits oncostatic activity against neoplastic cells, including breast cancer.
- This study investigates melatonin's impact on human androgen-independent prostate cancer (DU 145) cells.
- The research aims to elucidate the mechanism behind melatonin's action on these cancer cells.
Purpose of the Study:
- To evaluate the effects of melatonin on the proliferation of DU 145 prostate cancer cells.
- To analyze melatonin's influence on the cell cycle distribution of DU 145 cells.
- To explore the potential mechanisms of melatonin's action, including receptor expression and localization.
Main Methods:
- Cell proliferation assessed via hemocytometer counts.
- Cell cycle distribution analyzed using Fluorescence-Activated Cell Sorting (FACS).
- Melatonin receptor (Mel(1a), Mel(1b)) expression detected by RT-PCR; binding sites investigated using radioreceptor assays and nuclear/membrane extracts; intracellular cAMP levels measured.
Main Results:
- Physiological doses of melatonin significantly inhibited DU 145 cell proliferation.
- Melatonin induced cell cycle arrest in the G0/G1 phase.
- While Mel(1a) mRNA was present, membrane receptor binding was undetectable; however, nuclear extracts showed melatonin binding sites, suggesting nuclear mediation.
Conclusions:
- Melatonin demonstrates direct oncostatic activity against human androgen-independent prostate cancer cells.
- Melatonin affects cancer cell cycle progression, leading to growth inhibition.
- The antiproliferative effects of melatonin in these cells are likely mediated by nuclear receptors.
