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Accepted Preprint first posted online on 30 September 2008

Endocrine-Related Cancer 2008;15:1003.

DOI: 10.1677/ERC-08-0125
Copyright © 2008 by the Society for Endocrinology.
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RESEARCH

Signalling pathways involved in the antiproliferative effect of molecular iodine in normal and tumoral breast cells: evidence that 6-iodolactone mediates apoptotic effects

 Omar Arroyo-Helguera, Emilio Rojas, Guadalupe Delgado and Carmen Aceves

O Arroyo-Helguera, Instituto de Neurobiologia, UNAM-Juriquilla, Universidad Nacional Autonoma de Mexico, Juriquilla, Mexico
E Rojas, Instituto de Investigaciones Biomedicas, Universidad Nacional Autonoma de Mexico, Mexico City, Mexico
G Delgado, Instituto de Neurobiologia, UNAM-Juriquilla, Universidad Nacional Autonoma de Mexico, Queretaro, Mexico
C Aceves, Instituto de Neurobiologia, UNAM-Juriquilla, Univesidad Nacional Autonoma de Mexico, Juriquilla, 76230, Mexico

Correspondence: Carmen Aceves, Email: caracev{at}servidor.unam.mx

Abstract

Previous reports have documented the antiproliferative properties of molecular iodine (I2) and the arachidonic acid (AA) derivative 6-iodolactone (6-IL) in both thyroid and mammary gland. In this study, we characterized the cellular pathways activated by these molecules and their effects on cell cycle arrest and apoptosis in normal (MCF-12F) and cancerous (MCF-7) breast cells. Low to moderate concentrations of I2 (10-20 µM) cause G1 and G2/M phase arrest in MCF-12F, and caspase-dependent apoptosis in MCF-7 cells. In normal cells, only high doses of I2 (40 µM) induced apoptosis, and this effect was mediated by poly (ADP-ribose) polymerase-1 (PARP-1) and the apoptosis-induced factor (AIF), suggesting an oxidative influence of iodine at high concentrations. Our data indicate that both I2 and 6-IL trigger the same intracellular pathways and suggest that the antineoplasic effect of I2 in mammary cancer involves the intracellular formation of 6-IL. Mammary cancer cells are known to contain high concentrations of arachidonic acid, which might explain why I2 exerts apoptotic effects at lower concentrations only in tumoral cells.






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Copyright © 2008 by the Society for Endocrinology.