Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
2019872 | Prostaglandins & Other Lipid Mediators | 2009 | 9 Pages |
Abstract
Recently we and other groups have shown that molecular iodine (I2) exhibits potent antiproliferative and apoptotic effects in mammary cancer models. In the human breast cancer cell line MCF-7, I2 treatment generates iodine-containing lipids similar to 6-iodo-5-hydroxy-eicosatrienoic acid and the 6-iodolactone (6-IL) derivative of arachidonic acid (AA), and it significantly decreases cellular proliferation and induces caspase-dependent apoptosis. Several studies have shown that AA is a natural ligand of the peroxisome proliferator-activated receptors (PPARs), which are nuclear transcription factors thought to participate in regulating cancer cell proliferation. Our results show that in MCF-7 cells: (1) 6-IL binds specifically and with high affinity to PPAR proteins (EMSA assays), (2) 6-IL activates both transfected (by transactivation assays) and endogenous (by lipid accumulation) peroxisome proliferator response elements, and (3) 6-IL supplementation increases PPARγ and decreases PPARα expression. These results implicate PPARs in a molecular mechanism by which I2, through formation of 6-IL, inhibits the growth of human breast cancer cells.
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Authors
R.E. Nuñez-Anita, O. Arroyo-Helguera, M. Cajero-Juárez, L. López-Bojorquez, C. Aceves,