Abstract

Introduction

Materials & Methods

Results

Discussion & Conclusion

References

Discussion
Board

Most explanations for the antitumoral effects of melatonin refer to the antiproliferative actions of this pineal hormone. However, tumor growth should be considered as a balance between cell proliferation and cell death. On this basis, we studied whether melatonin may play a role in the control of programmed cell death in MCF-7 human breast cancer cells. We found that melatonin, at physiological doses, increases the percentage of dead cells (evaluated by the trypan blue exclusion test). Furthermore, in situ labeling of apoptosis-induced DNA strand breaks by the TUNEL reaction showed that melatonin is able to activate apoptotic cell death in this tumoral cell line. The expression of both p53 and WAF1 genes in MCF-7 cells was also increased by nanomolar concentrations of melatonin. These findings support the hypothesis that melatonin treatment increases the number of MCF-7 cells which fall into apoptosis, probably by interacting with p53 mediated mechanisms.

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Poster Number PAcos0712
Keywords: MCF-7 cells, Melatonin, Apoptosis, p53, WAF1