Aceves article on I2 versus KI in breast cancer cells

[Guest guest]

New article on breast cancer animal models and Isub2 versus potassium

iodide.

The breast cancer cells took up I(2) independent of the NIS symporter

and retained a small amount of it (10%), unlike the control cells.

son

Endocr Relat Cancer. 2006 Dec;13(4):1147-58.

Uptake and antiproliferative effect of molecular iodine in the MCF-7

breast cancer cell line.

Arroyo-Helguera O, Anguiano B, Delgado G, Aceves C.

This study analyzes the uptake and antiproliferative effect of two

different chemical forms of iodine, iodide (I(-)) and molecular iodine

(I(2)), in MCF-7 cells, which are inducible for the Na(+)/I(-)

symporter (NIS) and positive for pendrin (PDS). The mouse fibroblast

cell line NIH3T3 was used as control. Our results show that in MCF-7

cells, I(-) uptake is sustained and dependent on NIS, whereas I(2)

uptake is transient with a maximal peak at 10 min and a final

retention of 10% of total uptake. In contrast, no I(-) was taken up by

NIH3T3 cells, and although I(2) was captured with the same time

pattern as in MCF-7 cells, its uptake was significantly lower, and it

was not retained within the cell. The uptake of I(2) is independent of

NIS, PDS, Na(+), and energy, but it is saturable and dependent on

protein synthesis, suggesting a facilitated diffusion system.

Radioiodine was incorporated into protein and lipid fractions only

with I(2) treatment. The administration of non-radiolabeled I(2) and

6-iodo-5-hydroxy-8,11,14-eicosatrienoic acid (6-iodolactone, an

iodinated arachidonic acid), but not KI, significantly inhibited

proliferation of MCF-7 cells. Proliferation of NIH3T3 cells was not

inhibited by 20 muM I(2). In conclusion, these results demonstrate

that I(2) uptake does not depend on NIS or PDS; they suggest that in

mammary cancer cells, I(2) is taken up by a facilitated diffusion

system and then covalently bound to lipids or proteins that, in turn,

inhibit proliferation.

PMID: 17158760