State of the Evidence: The Connection Between Breast Cancer and the Environment

Gray, Janet; Evans, Nancy Remage; Taylor, Brynn; Rizzo, Jeanne; Walker, Marisa

doi:10.1179/oeh.2009.15.1.43

Cited by 82 publications

(61 citation statements)

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“…[28][29][30] The presence of high concentrations of estrogen in breast tissue increases the risk of developing breast cancer and the ability of immature breast tissue cells to strongly bind to carcinogens, decreasing their DNA repair capacity. 31,32) Aromatase, a CYP19 enzyme, is the rate-limiting enzyme in the conversion of testosterone and androstenedione to the estrogens, estrone and estradiol. [26][27][28][29][30][32][33][34] It is involved in the final step of the estrogen biosynthetic pathway and its selective inhibition will not affect the production of other steroids in the pathway.…”

Section: Resultsmentioning

confidence: 99%

Aromatase Inhibitory Activity of Geranylated Coumarins, Mammeasins C and D, Isolated from the Flowers of <i>Mammea siamensis</i>

et al. 2016

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Key words Mammea siamensis; mammeasin; aromatase inhibitor; geranylated coumarin; Calophyllaceae Mammea siamensis (MIQ.) T. ANDERS. is a species of flowering plant in the Calophyllaceae family and is widely distributed in Thailand, Laos, Cambodia, Vietnam, and Myanmar. The flowers of this plant have been used for preparing a heart tonic in Thai traditional medicine ("Sarapi" in Thai). [1][2][3][4][5][6][7][8][9][10] Several coumarins, [1][2][3][4][5][6][7] xanthones, 8,9) triterpenoids, 10) and steroids 10) have been isolated from the flowers, 1,2,6,7,10) seeds, 3,9) twigs, 4,8) and bark 5) of this plant. In the course of our characterization studies on bioactive constituents in Thai natural medicine, 1,[11][12][13][14][15][16][17][18][19][20][21][22][23][24][25] we reported that the methanol extract of the flowers of M. siamensis and its coumarin constituents showed inhibitory effects on nitric oxide production in lipopolysaccharide-activated RAW264.7 cells.1) Further studies revealed that the methanol extract inhibited enzymatic activity against aromatase. Separation of the active constituents in the extract allowed us to isolate two new geranylated coumarins, mammeasins C (1) and D (2). This paper describes the isolation and structure elucidation of these new coumarins (1, 2) and the inhibitory effects of the coumarin constituents (1-26) on aromatase. 26) Results and Discussion Effects of the Methanol Extract from the Flowers of M. siamensis against Human Recombinant AromataseBreast cancer is one of the most common reasons for mortality in women. 26,27) Estrogens and estrogen receptors are well known to play an important role in the development and progression of hormone-dependent breast cancer; for this reason, estrogens and estrogen receptors are widely studied molecular targets. [28][29][30] The presence of high concentrations of estrogen in breast tissue increases the risk of developing breast cancer and the ability of immature breast tissue cells to strongly bind to carcinogens, decreasing their DNA repair capacity. 31,32) Aromatase, a CYP19 enzyme, is the rate-limiting enzyme in the conversion of testosterone and androstenedione to the estrogens, estrone and estradiol. [26][27][28][29][30][32][33][34] It is involved in the final step of the estrogen biosynthetic pathway and its selective inhibition will not affect the production of other steroids in the pathway. 32,[35][36][37] The source of estrogen production in breast cancer tissues is intratumoral aromatase, and thus, inhibition of aromatase may inhibit the growth stimulation effect of estrogens in breast cancer tissues. Therefore, aromatase is considered a useful therapeutic target in the treatment and prevention of estrogen-dependent breast cancer. 32)The dried flowers of M. siamensis (collected from Nakhonsithammarat Province, Thailand) were extracted with methanol under reflux (25.66% from the dried flowers). The methanol extract was partitioned into an EtOAc-H 2 O (1 : 1, v/v) mixture to furnish an EtOAc-soluble fraction (6.84%) and an aqueous ...

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Section: Resultsmentioning

confidence: 99%

Aromatase Inhibitory Activity of Geranylated Coumarins, Mammeasins C and D, Isolated from the Flowers of <i>Mammea siamensis</i>

et al. 2016

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“…1, endocrine disruptors that mimic or antagonize endogenous estrogens are relevant to breast cancer. Estrogen-like compounds include pesticides, industrial chemicals, pharmaceuticals, and plant-derived compounds, all of which can expose humans through food or water supply (Gray et al 2009). Many are lipophilic and can be stored in adipose tissue.…”

Section: Prl and Chemoresistancementioning

confidence: 99%

“…Although the general belief is that long-term consumption of phytoestrogens (i.e. soy products) helps in reducing a woman's risk of breast cancer, this notion is controversial (Martin et al 2007, Gray et al 2009). …”

Section: Prl and Chemoresistancementioning

confidence: 99%

Novel roles of prolactin and estrogens in breast cancer: resistance to chemotherapy

LaPensee

Ben‐Jonathan

2010

Endocrine-Related Cancer

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Resistance to chemotherapy is a major complication in the treatment of advanced breast cancer. Estrogens and prolactin (PRL) are implicated in the pathogenesis of breast cancer but their roles in chemoresistance have been overlooked. A common feature to the two hormones is activation of their receptors by diverse compounds, which mimic or antagonize their actions. The PRL receptor is activated by lactogens (PRL, GH, or placental lactogen) originating from the pituitary, breast, adipose tissue, or the placenta. Estrogen receptors exist in multiple membrane-associated and cytoplasmic forms that can be activated by endogenous estrogens, man-made chemicals, and phytoestrogens. Here, we review evidence that low doses of PRL, estradiol (E 2 ), and bisphenol A (BPA) antagonize multiple anticancer drugs that induce cell death by different mechanisms. Focusing on cisplatin, a DNA-damaging drug which is effective in the treatment of many cancer types but not breast cancer, we compare the abilities of PRL, E 2 , and BPA to antagonize its cytotoxicity. Whereas PRL acts by activating the glutathione-S-transferase detoxification enzyme, E 2 and BPA act by inducing the antiapoptotic protein Bcl-2. The implications of these findings to patients undergoing chemotherapy are discussed.

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“…developmental and metabolic disorders, reproductive disturbances, and malignant tumors (9)(10)(11)(12)(13)(14). Children are especially susceptible to adverse effects of EED exposure due to their physiological characteristics such as small body size and limited capacity to metabolize EED (9,10).…”

Section: Environmental Endocrine Disruptors Promote Invasion and Metamentioning

confidence: 99%

Environmental endocrine disruptors promote invasion and metastasis of SK-N-SH human neuroblastoma cells

Xiao¹

2009

Oncol Rep

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Abstract. Neuroblastoma (NB) is the most common pediatric extracranial cancer. Metastasis is the main cause of mortality in NB patients. Currently, little is known about the risk factors and their mechanisms that cause metastasis. Environmental endocrine disruptors (EED) are recently identified risk factors associated with various human diseases including malignant tumors. Our previous studies have implicated the role of di(2-ethylhexyl) phthalate (DEHP) and bisphenol A (BPA), two of the most common EED, in neuroblastoma cell proliferation. Here, we further investigated the effects of DEHP, BPA as well as 17ß-estradiol (E 2 ) on the invasion and metastasis of human neuroblastoma SK-N-SH cells in vitro. SK-N-SH cells expressed estrogen receptor (ER)-ß, matrix metalloproteinases-2 (MMP-2), MMP-9 and tissue inhibitor of matrix metalloproteinase-2 (TIMP-2) at readily detectable levels. 50 μM DEHP, 0.1 μM BPA and 10 μM E 2 exposure all resulted in enhanced motility and invasiveness of SK-N-SH cells (P<0.001), elevated expression of MMP-2 and MMP-9, and decreased expression of TIMP-2 (P<0.01). Furthermore, phosphorylation of Akt (Ser473) was also induced following the exposure (P<0.01). Importantly, both ER antagonist ICI182,780 and phosphoinositide 3-kinase (PI3K) specific inhibitor LY294002 significantly inhibited the DEHP, BPA, or E 2 -induced cell migration and invasion, as well as the disregulation of MMP-2, MMP-9 and TIMP-2 expression. ICI182,780 may have worked through abolishing Akt (Ser473) phosphorylation. In conclusion, DEHP, BPA, and E 2 potently promote invasion and metastasis of neuroblastoma cells through overexpression of MMP-2 and MMP-9 as well as downregulation of TIMP-2. ER-dependent pathway and PI3K/Akt pathway are involved, which may become potential therapeutic targets for neuroblastoma treatment.

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State of the Evidence: The Connection Between Breast Cancer and the Environment

Cited by 82 publications

References 0 publications

Aromatase Inhibitory Activity of Geranylated Coumarins, Mammeasins C and D, Isolated from the Flowers of <i>Mammea siamensis</i>

Aromatase Inhibitory Activity of Geranylated Coumarins, Mammeasins C and D, Isolated from the Flowers of <i>Mammea siamensis</i>

Novel roles of prolactin and estrogens in breast cancer: resistance to chemotherapy

Environmental endocrine disruptors promote invasion and metastasis of SK-N-SH human neuroblastoma cells

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