Iodine Alters Gene Expression in the MCF7 Breast Cancer Cell Line: Evidence for an Anti-Estrogen Effect of Iodine

Stoddard, Frederick R.; Brooks, Ari D.; Eskin, Bernard A.; Johannes, Gregg J.

doi:10.7150/ijms.5.189

Cited by 60 publications

(54 citation statements)

References 46 publications

(47 reference statements)

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“…Some of the primary risk factors for female breast cancer include age (2), lack of childbearing or breastfeeding (3), high hormone levels (e.g., estrogen) (4), and ethnicity (5). However, diet is another important factor that contributes to the development of breast cancer (6)(7)(8). The impact of diet on the incidence of breast cancer is indicated by geographic differences in the occurrence of the disease (9), and by the many dietary components experimentally proven to act as antibreast cancer agents.…”

Section: Introductionmentioning

confidence: 99%

Diallyl Disulfide-Induced Apoptosis in a Breast-Cancer Cell Line (MCF-7) May Be Caused by Inhibition of Histone Deacetylation

Altonsy

Habib

Andrews

2012

Nutrition and Cancer

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The health benefits of garlic have been proven by epidemiological and experimental studies. Diallyl disulphide (DADS), the major organosulfur compound found in garlic oil, is known to lower the incidence of breast cancer both in vitro and in vivo. The studies reported here demonstrate that DADS induces apoptosis in the MCF-7 breast-cancer cell line through interfering with cell-cycle growth phases in a way that increases the sub-G(0) population and substantially halts DNA synthesis. DADS also induces phosphatidylserine translocation from the inner to the outer leaflet of the plasma membrane and activates caspase-3. Further studies revealed that DADS modulates the cellular levels of Bax, Bcl-2, Bcl-xL, and Bcl-w in a dose-dependent manner, suggesting the involvement of Bcl-2 family proteins in DADS induced apoptosis. Histone deacetylation inhibitors (HDACi) are known to suppress cancer growth and induce apoptosis in cancer cells. Here it is shown that DADS has HDACi properties in MCF-7 cells as it lowers the removal of an acetyl group from an acetylated substrate and induces histone-4 (H4) hyper-acetylation. The data thus indicate that the HDACi properties of DADS may be responsible for the induction of apoptosis in breast cancer cells.

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Section: Introductionmentioning

confidence: 99%

Diallyl Disulfide-Induced Apoptosis in a Breast-Cancer Cell Line (MCF-7) May Be Caused by Inhibition of Histone Deacetylation

Altonsy

Habib

Andrews

2012

Nutrition and Cancer

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“…Iodine may also be affecting the binding of estrogen receptors to the steroid-binding element. Using breast cancer cells (MCF-7 cells), Stoddard and colleagues demonstrated that Lugol's solution (5% iodine/10% iodide) affected 43 genes involved cell cycle growth, proliferation, and differentiation [19]. Many of the 43 genes are those up regulated by estrogens, implying that the Lugol's solution interfered with this action and had a net "anti-estrogenic" effect on gene expression.…”

Section: Discussionmentioning

confidence: 99%

Iodine Deficieency and Its Proliferation in Cancer Increase

Emmanuel¹,

Oliver²,

Angela³

2016

AJLSR

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Iodine is an essential element in human physiology. It's well known to play vital role in thyroid functions. However it has been updated to be the most important element with the highest percentage of demand by the human body. This is because iodine is the heaviest and richest in electrons among required elements in the animal diet. Inorganic iodides are necessary for all living vegetable and animal cells, but only the vertebrates have the thyroid gland and its iodinated hormones. In humans, the total amount of iodine is about 30-50 mg and less than 30% is present in thyroid gland and its hormones. About 60-80% of total iodine is non-hormonal as contained in its extrathyroidal tissues. Dietary iodine deficiency is associated with the development of mammary pathology and cancer. Mammary gland embryogenetically derived from primitive iodide-concentrating ectoderma, and alveolar and ductular cells of the breast specialize in uptake and secretion of iodine in milk in order to supply offsrings with this important trace-element. Breast and thyroid share an important iodide-concentrating ability and an efficient peroxidase activity, which transfers electrons from iodides to the oxygen of hydrogen peroxide, forming iodoproteins and iodolipids, and so protect the cells from peroxidative damage. Thyroid nodules are a common clinical problem, and differentiated thyroid cancer is becoming increasingly prevalent. The aim of these guidelines is to inform clinicians, patients, researchers, and health policy makers on published evidence relating to the diagnosis and management of thyroid nodules and differentiated thyroid cancer.

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“…It is well-documented that molecular iodine (I 2 ) has a potent antitumor effect on mammary cancer in rats via regulating the cell oxidative environment (25). A gene array study showed that PVP-I inhibits breast cancer (MCF-7) through modulation of the estrogen pathway (26). Moreover, Shrivastava et al (27) have showed that iodine induced human breast cancer cell (MCF-7) death through activating a caspase-independent and mitochondria-mediated apoptotic pathway.…”

Section: Discussionmentioning

confidence: 99%

Diluted povidone-iodine inhibits tumor growth through apoptosis-induction and suppression of SOD activity

Zhao

2011

Oncol Rep

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Abstract. Povidone-iodine (PVP-I) is widely used in clinical practice as an antiseptic and flushing agent after surgery to remove a tumor. Our present study was designed to determine whether diluted PVP-I is cytotoxic to colon cancer cells and ascetic tumor cells in vitro and to examine its antitumor effects in vivo. In vitro, CT26 and H22 cells treated with different concentrations of diluted PVP-I (0-1.56 µg/ml) were analyzed using the mononuclear cell direct cytotoxicity assay (MTT) and a flow cytometry assay. In vivo, Balb/c mice injected in the abdominal cavity with CT26 cells or H22 cells were treated intraperitoneally with different concentrations of PVP-I (0-312.5 µg/mouse), cisplatin (40 mg/kg) or 5'-FU (30 mg/kg) or left untreated. In vitro, the studies demonstrated the antiproliferative and significant apoptosis-inducing effects of PVP-I in a dose-and time-dependent manner. In vivo, PVP-I significantly repressed the growth of H22 and CT26 cells in Balb/c mice compared to controls. To explore the mechanism of the antitumor effect of PVP-I, the superoxide dismutase (SOD) activity of ascites extracted from a mouse model and the supernatant of CT26 cells was detected by an SOD kit. The activity of SOD was significantly inhibited in the experimental groups. Taken together, our data suggest that PVP-I exhibits a strong inhibitory effect on tumor growth in colon cancer (CT26) and hepatoma (H22) resulting from apoptosis, both in vitro and in vivo, suggesting a new potential therapeutic approach after tumor excision surgery to colon cancer and hepatoma. IntroductionColorectal cancer and hepatoma, the most common malignant tumors worldwide, are responsible for a great number of cancer deaths (1-4). Excisional surgery, the most effective therapy in achieving cure, plays an important part in the management of these cancers (5). Owing to port-site metastases, the benefits of laparoscopic surgery which is the primary treatment modality for colorectal cancer are uncertain (6). Balli et al (7) have described a technique for preventing port-site metastases based on their 8-year experience with laparoscopic surgery for colorectal cancer. In this 6-step technique use of 5% povidoneiodine (PVP-I) intraluminal irrigation and intraoperative colonoscopy are an important routine (7). Moreover, another laparoscopic experimental study showed that the PVP-I solution resulted in almost zero implantation rate at trocar sites, as compared with other cytotoxic agents (8). These findings suggest that PVP-I probably has anti-tumor activity.PVP-I, a broad spectrum microbicide against bacteria, virus, fungi and parasites in vitro (9-12), consists of elementary iodine bound to the carrier poly (1-vinyl-2-pyrrolidone) that enhances the solubility and gives a depot of iodine (13). Based on the oxidizing effects of free iodine on NH-and SH-OH-groups of amino acids and on double bonds of unsaturated fatty acids, PVP-I showed the ability of non-specifically inducing cell death (14). Previous studies have demonstrated that PVP-I had anti-tumo...

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Iodine Alters Gene Expression in the MCF7 Breast Cancer Cell Line: Evidence for an Anti-Estrogen Effect of Iodine

Cited by 60 publications

References 46 publications

Diallyl Disulfide-Induced Apoptosis in a Breast-Cancer Cell Line (MCF-7) May Be Caused by Inhibition of Histone Deacetylation

Diallyl Disulfide-Induced Apoptosis in a Breast-Cancer Cell Line (MCF-7) May Be Caused by Inhibition of Histone Deacetylation

Iodine Deficieency and Its Proliferation in Cancer Increase

Diluted povidone-iodine inhibits tumor growth through apoptosis-induction and suppression of SOD activity

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