Antineoplastic effect of iodine in mammary cancer: participation of 6-iodolactone (6-IL) and peroxisome proliferator-activated receptors (PPAR)

Aceves, Carmen; García‐Solís, Pablo; Arroyo-Helguera, Omar; Vega-Riveroll, Laura; Delgado, Gabriela; Anguiano, Brenda

doi:10.1186/1476-4598-8-33

Cited by 48 publications

(54 citation statements)

References 32 publications

(38 reference statements)

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“…In extrathyroid tissues, iodine plays an important role in the redox balance, either by free radical competition or indirectly inducing antioxidant enzymes, mediated by PPAR-gamma transcription factor activated by iodolactones. This ligand has been reported as iodine mediator [12,13,15,16,20,21]. Adequate iodine supplement is important for normal pregnancy, as iodine deficiency has been associated with oxidative stress and pregnant complications such as preeclampsia [22][23][24].…”

Section: Introductionmentioning

confidence: 98%

“…In the thyroid gland, intracellular iodine concentration plays an important role in redox balance by modulating hydrogen peroxide generation [8,9] and thyroid iodine deficiency induced intracellular production of reactive oxygen species (ROS) that stabilizes HIF-1α protein and then the expression and secretion of vascular epithelial growth factor (VEGF) for novel blood vessels [10]. It has been proposed that in thyroid and extrathyroid tissues, iodolipids are the mediators of iodine properties, through PPAR-gamma activation [11][12][13][14][15][16].…”

Section: Introductionmentioning

confidence: 99%

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Iodine Affects Differentiation and Migration Process in Trophoblastic Cells

Vidal

Rodríguez

Arroyo-Helguera

2015

Biol Trace Elem Res

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Iodine deficiency is associated with oxidative stress increase and preeclampsia during gestation, suggesting that iodine concentration plays an important role in the normal placenta physiology. The question raised is to analyze the effect of iodine deficiency on oxidative stress, viability, differentiation, and migration process and changes in the expression of differentiation and migration markers. Iodine deprivation was done using potassium perchlorate (KCLO4) to block sodium iodide symporter (NIS) transporter and 4,4'-diisothiocyanatostilbene-2,2'-disulfonic acid DIDS to inhibit pendrine (PEN) transport for 3-48 h. Then trophoblast cells were treated with low iodine doses of 5-500 μM and high iodine doses of 100-5000 μM. Oxidative stress, viability, and human chorionic gonadotropin (hGC) were measured by colorimetric methods. Migration throphoblast cells were evaluated by both wound healing and Boyden chamber assays. Changes in mRNA expression were analyzed by real-time RT-PCR. Iodine deprivation induces a significant increase of reactive oxygen species (ROS), viability, and migration process vs control cells. We found a significant overregulation in the mRNA's peroxisome proliferator-activated receptor (PPAR-gamma), Snail, and matrix metalloproteinase-9 (MMP-9) mRNA's in cells deprived of iodine, as well as a down glial cell missing-1 (GCM-1) regulation, hGC, pregnancy-associated plasma protein-A (PAPP-A), and E-cadherin mRNA expression. The expression of hypoxic induction factor alpha (HIFα) mRNA does not change with iodine deprivation. In cells deprived of iodine, supplementing low iodine doses (5-500 μM) does not induce any significant changes in viability. However, ROS and migration process were decreased, although we found an increased human chorionic gonadotropin (hCG) secretion as a differentiation marker. In addition, we found that PPAR-gamma, Snail, and MPP-9 mRNAs expression are downregulated with low iodine doses, in contrast with GCM-1, PAPP-A, hGC, and E-cadherin that increase their expression vs cells deprived of iodine. High iodine doses (1000-5000 μM) have shown cytotoxic effects. Based on our results, iodine is important for keeping the proliferation/differentiation balance in the placenta.

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Section: Introductionmentioning

confidence: 98%

Section: Introductionmentioning

confidence: 99%

Iodine Affects Differentiation and Migration Process in Trophoblastic Cells

Vidal

Rodríguez

Arroyo-Helguera

2015

Biol Trace Elem Res

Self Cite

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“…In breast cancer models, it has been shown that iodine supplementation inhibits expression of the VEGF and uPA genes (13,14). Our study shows that none of the TRAMP mice (control or iodine supplemented) developed a phenotype of The amount of mono-and oligo-nucleosomes was determined by ELISA.…”

Section: R E S E a R C H A R T I C L Ementioning

confidence: 88%

“…This result could be explained by a strong inactivation of the p53 pathway by TAG antigens. for peroxisome proliferator-activated receptors (12,13,(18)(19)(20). There is evidence that prostate epithelium is an iodine-responsive target.…”

Section: Introductionmentioning

confidence: 99%

“…It is well established that I -uptake depends on the Na + /I -symporter (NIS), whereas the uptake of I 2 is probably mediated by facilitated diffusion (6)(7)(8). I 2 supplementation exerts antitumor effects in thyroid, breast, neuroblastoma and lung carcinoma by arresting the cell cycle (increases p53 and p21 proteins), inducing apoptosis (dissipates mitochondrial membrane potential and increases Bax, caspases 3 and 7) and reducing mRNA expression of invasion genes (vascular endothelial growth factor [VEGF] and urokinase-type plasminogen activator [uPA]) (9)(10)(11)(12)(13)(14). For I -to exert some of these effects, it must be converted to an oxidized species of iodine by specific peroxidases (thyro-, lacto-or myeloperoxidase) (15)(16)(17).…”

Section: Introductionmentioning

confidence: 99%

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