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      KCI등재

      Effect of Natural Compounds on Catechol Estrogen-Induced Carcinogenesis

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      https://www.riss.kr/link?id=A106109513

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      다국어 초록 (Multilingual Abstract)

      The hydroxylation of estradiol results in the formation of catechol estrogens such as 2-hydroxyestradiol (2-OHE2) and 4-hydroxyestradiol (4-OHE2). These catechol estrogens are further oxidized to quinone metabolites by peroxidases or cytochrome P450 (...

      The hydroxylation of estradiol results in the formation of catechol estrogens such as 2-hydroxyestradiol (2-OHE2) and 4-hydroxyestradiol (4-OHE2). These catechol estrogens are further oxidized to quinone metabolites by peroxidases or cytochrome P450 (CYP450) enzymes. Catechol estrogens contribute to hormone-induced carcinogenesis by generating DNA adducts or reactive oxygen species (ROS). Interestingly, many of the natural products found in living organisms have been reported to show protective effects against carcinogenesis induced by catechol estrogens. Although some compounds have been reported to increase the activity of catechol estrogens via oxidation to quinone metabolites, many natural products decreased the activity of catechol estrogens by inhibiting DNA adduct formation, ROS production, or oxidative cell damage. Here we focus specifically on the chemopreventive effects of these natural compounds against carcinogenesis induced by catechol estrogens.

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      참고문헌 (Reference)

      1 Mense SM, "Vitamin C and alpha-naphthoflavone prevent estrogen-induced mammary tumors and decrease oxidative stress in female aci rats" 30 : 1202-1208, 2009

      2 Lareef MH, "The estrogen antagonist ici-182-780 does not inhibit the transformation phenotypes induced by 17-beta-estradiol and 4-oh estradiol in human breast epithelial cells" 26 : 423-429, 2005

      3 MacLusky NJ, "The catechol estrogens" 15 : 111-124, 1981

      4 Lehmann L, "Soy isoflavones decrease the catechol-o-methyltransferase-mediated inactivation of 4-hydroxyestradiol in cultured mcf-7 cells" 29 : 363-370, 2008

      5 Takemura H, "Selective inhibition of methoxyflavonoids on human cyp1b1 activity" 18 : 6310-6315, 2010

      6 Park SA, "Resveratrol suppresses 4-hydroxyestradiol -induced transformation of human breast epithelial cells by blocking ikappab kinasebeta-nf-kappab signalling" 46 : 1051-1057, 2012

      7 Zhou X, "Resveratrol represses estrogen-induced mammary carcinogenesis through nrf2- ugt1a8-estrogen metabolic axis activation" 155 : 252-263, 2018

      8 Lu F, "Resveratrol prevents estrogen-DNA adduct formation and neoplastic transformation in mcf-10f cells" 1 : 135-145, 2008

      9 Chen ZH, "Resveratrol inhibits tcdd-induced expression of cyp1a1 and cyp1b1 and catechol estrogen-mediated oxidative DNA damage in cultured human mammary epithelial cells" 25 : 2005-2013, 2004

      10 Zahid M, "Resveratrol and n-acetylcysteine block the cancer-initiating step in mcf-10f cells" 50 : 78-85, 2011

      1 Mense SM, "Vitamin C and alpha-naphthoflavone prevent estrogen-induced mammary tumors and decrease oxidative stress in female aci rats" 30 : 1202-1208, 2009

      2 Lareef MH, "The estrogen antagonist ici-182-780 does not inhibit the transformation phenotypes induced by 17-beta-estradiol and 4-oh estradiol in human breast epithelial cells" 26 : 423-429, 2005

      3 MacLusky NJ, "The catechol estrogens" 15 : 111-124, 1981

      4 Lehmann L, "Soy isoflavones decrease the catechol-o-methyltransferase-mediated inactivation of 4-hydroxyestradiol in cultured mcf-7 cells" 29 : 363-370, 2008

      5 Takemura H, "Selective inhibition of methoxyflavonoids on human cyp1b1 activity" 18 : 6310-6315, 2010

      6 Park SA, "Resveratrol suppresses 4-hydroxyestradiol -induced transformation of human breast epithelial cells by blocking ikappab kinasebeta-nf-kappab signalling" 46 : 1051-1057, 2012

      7 Zhou X, "Resveratrol represses estrogen-induced mammary carcinogenesis through nrf2- ugt1a8-estrogen metabolic axis activation" 155 : 252-263, 2018

      8 Lu F, "Resveratrol prevents estrogen-DNA adduct formation and neoplastic transformation in mcf-10f cells" 1 : 135-145, 2008

      9 Chen ZH, "Resveratrol inhibits tcdd-induced expression of cyp1a1 and cyp1b1 and catechol estrogen-mediated oxidative DNA damage in cultured human mammary epithelial cells" 25 : 2005-2013, 2004

      10 Zahid M, "Resveratrol and n-acetylcysteine block the cancer-initiating step in mcf-10f cells" 50 : 78-85, 2011

      11 Yang L, "Reduced formation of depurinating estrogen-DNA adducts by sulforaphane or keap1 disruption in human mammary epithelial mcf-10a cells" 34 : 2587-2592, 2013

      12 Zitka O, "Redox status expressed as gsh:Gssg ratio as a marker for oxidative stress in paediatric tumour patients" 4 : 1247-1253, 2012

      13 Zahid M, "Prevention of estrogen-DNA adduct formation in mcf-10f cells by resveratrol" 45 : 136-145, 2008

      14 Mense SM, "Preferential induction of cytochrome p450 1a1 over cytochrome p450 1b1 in human breast epithelial cells following exposure to quercetin" 110 : 157-162, 2008

      15 Wagner J, "Phytoestrogens modulate the expression of 17alpha-estradiol metabolizing enzymes in cultured mcf-7 cells" 617 : 625-632, 2008

      16 van Duursen MB, "Phytochemicals inhibit catechol-o-methyltransferase activity in cytosolic fractions from healthy human mammary tissues: Implications for catechol estrogen-induced DNA damage" 81 : 316-324, 2004

      17 Jiang YL, "Natural products as anti-invasive and antimetastatic agents" 18 : 808-829, 2011

      18 Yuan G, "Natural products and anti-inflammatory activity" 15 : 143-152, 2006

      19 Cavalieri EL, "Molecular origin of cancer: Catechol estrogen-3,4-quinones as endogenous tumor initiators" 94 : 10937-10942, 1997

      20 Thompson PA, "Molecular epidemiology of genetic polymorphisms in estrogen metabolizing enzymes in human breast cancer" 125-134, 2000

      21 이은주, "Modulatory effects of α- and γ-tocopherols on 4-hydroxyestradiol induced oxidative stresses in MCF-10A breast epithelial cells" 한국영양학회 3 (3): 185-191, 2009

      22 Zahid M, "Inhibition of depurinating estrogen-DNA adduct formation by natural compounds" 20 : 1947-1953, 2007

      23 Borras C, "Genistein, a soy isoflavone, up-regulates expression of antioxidant genes: Involvement of estrogen receptors, erk1/2, and nfkappab" 20 : 2136-2138, 2006

      24 Zhu BT, "Functional role of estrogen metabolism in target cells: Review and perspectives" 19 : 1-27, 1998

      25 Gaikwad NW, "Evidence from esi-ms for nqo1-catalyzed reduction of estrogen ortho-quinones" 43 : 1289-1298, 2007

      26 Parl FF, "Estrogen metabolism and breast cancer: A risk model" 1155 : 68-75, 2009

      27 Xu X, "Effects of soy isoflavones on estrogen and phytoestrogen metabolism in premenopausal women" 7 : 1101-1108, 1998

      28 Moon YJ, "Dietary flavonoids: Effects on xenobiotic and carcinogen metabolism" 20 : 187-210, 2006

      29 Fussell KC, "Catechol metabolites of endogenous estrogens induce redox cycling and generate reactive oxygen species in breast epithelial cells" 32 : 1285-1293, 2011

      30 Cavalieri E, "Catechol estrogen quinones as initiators of breast and other human cancers: Implications for biomarkers of susceptibility and cancer prevention" 1766 : 63-78, 2006

      31 Ji Y, "Breast cancer risk reduction and membrane-bound catechol o-methyltransferase genetic polymorphisms" 68 : 5997-6005, 2008

      32 Pastore A, "Analysis of glutathione: Implication in redox and detoxification" 333 : 19-39, 2003

      33 Takemura H, "A methoxyflavonoid, chrysoeriol, selectively inhibits the formation of a carcinogenic estrogen metabolite in mcf-7 breast cancer cells" 118 : 70-76, 2010

      34 Dias DA, "A historical overview of natural products in drug discovery" 2 : 303-336, 2012

      35 Park SA, "4-hydroxyestradiol induces anchorage-independent growth of human mammary epithelial cells via activation of ikappab kinase: Potential role of reactive oxygen species" 69 : 2416-2424, 2009

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      학술지 이력

      학술지 이력
      연월일 이력구분 이력상세 등재구분
      2022 평가예정 재인증평가 신청대상 (재인증)
      2019-01-01 평가 등재학술지 유지 (계속평가) KCI등재
      2016-01-01 평가 등재학술지 선정 (계속평가) KCI등재
      2015-12-01 평가 등재후보로 하락 (기타) KCI등재후보
      2015-04-07 학술지명변경 외국어명 : Journal of Experimental and Biomedical Sciences -> Biomedical Science Letters KCI등재
      2011-03-29 학술지명변경 외국어명 : The Journal of Biomedical Laboratory Sciences -> Journal of Experimental and Biomedical Sciences KCI등재
      2011-01-01 평가 등재학술지 선정 (등재후보2차) KCI등재
      2010-01-01 평가 등재후보 1차 PASS (등재후보1차) KCI등재후보
      2009-01-01 평가 등재후보 1차 FAIL (등재후보1차) KCI등재후보
      2008-01-01 평가 등재후보학술지 유지 (등재후보1차) KCI등재후보
      2007-01-01 평가 등재후보학술지 유지 (등재후보1차) KCI등재후보
      2006-01-01 평가 등재후보 1차 FAIL (등재후보2차) KCI등재후보
      2005-01-01 평가 등재후보 1차 PASS (등재후보1차) KCI등재후보
      2003-07-01 평가 등재후보학술지 선정 (신규평가) KCI등재후보
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      학술지 인용정보

      학술지 인용정보
      기준연도 WOS-KCI 통합IF(2년) KCIF(2년) KCIF(3년)
      2016 0.4 0.4 0.32
      KCIF(4년) KCIF(5년) 중심성지수(3년) 즉시성지수
      0.23 0.19 0.347 0.18
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