Iodoprotein Formation by Rat Mammary Glands during Pregnancy and Early Postpartum Period

Shah, Noor Muhammad; Eskin, Bernard A.; Krouse, Theodore; Sparks, Charles E.

doi:10.3181/00379727-181-42279

Cited by 26 publications

(15 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Iodide organification is, therefore, one of the important factors for the thyroid gland to retain trapped iodide. In lactating mammary gland, and some hormonedependent mammary tumors, iodination of protein was observed (13,14,16). Our results of iodide organification, however, indicated no iodination activity in MCF-7 cells, whereas a small amount of iodide was organified in FRTL-5 cells.…”

Section: Discussioncontrasting

confidence: 43%

“…In the mouse lactating mammary gland, iodide is concentrated 6-to 15-fold in milk, relative to the plasma iodide concentration (13), less than the magnitude of iodine concentration in the thyroid. Trapped iodide is secreted into the milk, and Ϸ20% is organified, as a result of the action of peroxidase expressed in the alveolar cells of the breast (14)(15)(16). Recent studies have demonstrated expression of NIS in the mammary gland (17)(18)(19).…”

mentioning

confidence: 99%

See 1 more Smart Citation

Retinoic acid induces sodium/iodide symporter gene expression and radioiodide uptake in the MCF-7 breast cancer cell line

Kogai

Schultz

Johnson

et al. 2000

Proc. Natl. Acad. Sci. U.S.A.

127

133

View full text Add to dashboard Cite

show abstract

Section: Discussioncontrasting

confidence: 43%

mentioning

confidence: 99%

Retinoic acid induces sodium/iodide symporter gene expression and radioiodide uptake in the MCF-7 breast cancer cell line

Kogai

Schultz

Johnson

et al. 2000

Proc. Natl. Acad. Sci. U.S.A.

127

133

View full text Add to dashboard Cite

show abstract

“…Since metastatic tumors generally have an abundant blood supply, such tumors with sufficient NIS expression could be good candidates for radioiodide therapy. In the mammary gland, iodination of tyrosyl residues on caseins and other milk proteins correlates with peroxidase activity (Strum 1978, Shah et al 1986. Iodide organification may occur even in inactive breast tissues (Strum et al 1983).…”

Section: Iodide Organification and Iodide Retention In Thyroid And Brmentioning

confidence: 99%

Enhancement of sodium/iodide symporter expression in thyroid and breast cancer

Kogai¹,

Taki²,

Brent³

2006

Endocr Relat Cancer

170

150

View full text Add to dashboard Cite

The sodium/iodide symporter (NIS) mediates iodide uptake in the thyroid gland and lactating breast. NIS mRNA and protein expression are detected in most thyroid cancer specimens, although functional iodide uptake is usually reduced resulting in the characteristic finding of a 'cold' or non-functioning lesion on a radioiodine image. Iodide uptake after thyroid stimulating hormone (TSH) stimulation, however, is sufficient in most differentiated thyroid cancer to utilize b-emitting radioactive iodide for the treatment of residual and metastatic disease. Elevated serum TSH, achieved by thyroid hormone withdrawal in athyreotic patients or after recombinant human thyrotropin administration, directly stimulates NIS gene expression and/or NIS trafficking to the plasma membrane, increasing radioiodide uptake. Approximately 10-20% differentiated thyroid cancers, however, do not express the NIS gene despite TSH stimulation. These tumors are generally associated with a poor prognosis. Reduced NIS gene expression in thyroid cancer is likely due in part, to impaired trans-activation at the proximal promoter and/or the upstream enhancer. Basal NIS gene expression is detected in about 80% breast cancer specimens, but the fraction with functional iodide transport is relatively low. Lactogenic hormones and various nuclear hormone receptor ligands increase iodide uptake in breast cancer cells in vitro, but TSH has no effect. A wide range of 'differentiation' agents have been utilized to stimulate NIS expression in thyroid and breast cancer using in vitro and in vivo models, and a few have been used in clinical studies. Retinoic acid has been used to stimulate NIS expression in both thyroid and breast cancer. There are similarities and differences in NIS gene regulation and expression in thyroid and breast cancer. The various agents used to enhance NIS expression in thyroid and breast cancer will be reviewed with a focus on the mechanism of action. Agents that promote tumor differentiation, or directly stimulate NIS gene expression, may result in iodine concentration in 'scan-negative' thyroid cancer and some breast cancer.

show abstract

“…In mammary gland, I 2 but not I K supplementation alleviates human mastalgia (Ghent et al 1993, Kessler 2004) and exerts a potent antineoplasic effect on pharmaco-induced mammary tumoral progression in rats (Funahashi et al 1996, Garcia-Solis et al 2005. The lack of an I K effect has been explained by the fact that lactoperoxidase, the enzyme that oxidizes I K and covalently binds it to the milk protein casein, is expressed in normal lactating but not in tumoral mammary gland (Shah et al 1986, Anguiano et al 2007. Recently, we also showed that methylnitrosourea (MNU)-induced tumors contain fourfold more AA (the 6-IL precursor) than normal mammary glands, and that I 2 supplementation is accompanied by a tenfold higher 6-IL content in these tumors (Arroyo-Helguera et al 2006a).…”

Section: Introductionmentioning

confidence: 99%

“…It has been suggested that in thyroid gland the apoptotic iodide (I K ) effect is mediated by the derivatives of arachidonic acid (AA) or eicosapentaenoic acid such as 6-iodolactone (6-IL) or a-iodohexadecanal respectively (Dugrillon et al 1994, Langer et al 2003. The formation of these iodolipids requires, in addition to iodide uptake by specific transporters, its oxidation by thyroperoxidase (Shah et al 1986, Dohan et al 2003. In mammary gland, I 2 but not I K supplementation alleviates human mastalgia (Ghent et al 1993, Kessler 2004) and exerts a potent antineoplasic effect on pharmaco-induced mammary tumoral progression in rats (Funahashi et al 1996, Garcia-Solis et al 2005.…”

Section: Introductionmentioning

confidence: 99%

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

Arroyo-Helguera

Rojas²,

Delgado³

et al. 2008

Endocrine Related Cancer

View full text Add to dashboard Cite

Previous reports have documented the antiproliferative properties of I 2 and the arachidonic acid (AA) derivative 6-iodolactone (6-IL) in both thyroid and mammary glands. 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 I 2 (10-20 mM) 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 I 2 (40 mM) induced apoptosis, and this effect was mediated by poly (ADP-ribose) polymerase-1 (PARP1) and the apoptosis-induced factor, suggesting an oxidative influence of iodine at high concentrations. Our data indicate that both I 2 and 6-IL trigger the same intracellular pathways and suggest that the antineoplasic effect of I 2 in mammary cancer involves the intracellular formation of 6-IL. Mammary cancer cells are known to contain high concentrations of AA, which might explain why I 2 exerts apoptotic effects at lower concentrations only in tumoral cells.

show abstract

Iodoprotein Formation by Rat Mammary Glands during Pregnancy and Early Postpartum Period

Cited by 26 publications

References 0 publications

Retinoic acid induces sodium/iodide symporter gene expression and radioiodide uptake in the MCF-7 breast cancer cell line

Retinoic acid induces sodium/iodide symporter gene expression and radioiodide uptake in the MCF-7 breast cancer cell line

Enhancement of sodium/iodide symporter expression in thyroid and breast cancer

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

Contact Info

Product

Resources

About