Abstract
Estrogens are known for their proliferative effects, resulting in tumorigenesis and causing cancers. The majority of breast cancers are estrogen-dependent. Estrogenb-locking drugs developed for treating estrogen-dependent breast cancers include antagonists of estrogen receptors (ERs) and inhibitors of estrogen synthesis enzymes such as aromatase and steroid sulfatase (STS). However, drugs targeting estrogen inactivation enzyme, estrogen sulfotransferase (SULT1E1), have not been developed for estrogen-dependent cancer treatment or prevention. Estrogens must be inactivated after their actions in vivo by SULT1E1, uncontrolled estrogen activity in certain tissues will cause cancers. The majority of human breast cancer cell lines are known to express very low levels of SULT1E1 compared to normal mammary cells. Therefore, gene up-regulation of SULT1E1 could provide novel possibilities for the treatment of estrogen-dependent breast and endometrial cancers. Our data suggest that certain nutritional flavonoids induce SULT1E1 and inhibit cell proliferation in estrogen-dependent breast cancer MCF-7 cells. Our results also suggest that SULT1E1 inducer has an additive or synergistic effect on the inhibition of MCF-7 cell proliferation when combined with other known breast cancer drugs. Naturally occurring flavonoids are safe and inexpensive; they could be used for the prevention of certain breast cancers and/or used as co-drug for the treatment of estrogen-dependent cancers. These results may lead to creating innovative approaches for the treatment or prevention of estrogen-dependent cancers and may lead to the discovery of novel drugs or co-drugs.
Highlights
Cytosolic sulfotransferases (SULTs) catalyze the sulfation of endogenous and xenobiotic hydroxyl-containing compounds [1]
Our results suggest that SULT1E1 inducer has an additive or synergistic effect on the inhibition of MCF-7 cell proliferation when combined with other known breast cancer drugs
The results suggest that quercetin has the potential to be developed as an anti-estrogen-dependent cancer drug
Summary
Cytosolic sulfotransferases (SULTs) catalyze the sulfation of endogenous and xenobiotic hydroxyl-containing compounds [1]. Sulfation of xenobiotics is mainly associated with detoxification: sulfate esters are more water-soluble and more readily excreted by drug transporters than the parent compounds. SULTs are mostly studied as phase II drug-metabolizing enzymes. Some SULTs show exclusive endogenous substrate specificity; sulfation is widely observed in various biological processes. The biological activities of various biological signaling molecules, including hormones (hydroxysteroids, thyroids, and glucocorticoids) and monoamine neurotransmitters, can be altered through sulfation. Sulfation normally leads to the inactivation of biological signaling molecules, as the sulfated forms are typically unable to bind to specific receptors. Sulfatases catalyze the de-sulfation [2]; together with SULTs, they regulate the functions and activities of various molecules
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