重金属暴露与前列腺癌发生和进展的关系综述

李晓建, 潘东亮, 李宁忱, 刘思金. 重金属暴露与前列腺癌发生和进展的关系综述[J]. 环境化学, 2014, 33(10): 1776-1783. doi: 10.7524/j.issn.0254-6108.2014.10.015
引用本文: 李晓建, 潘东亮, 李宁忱, 刘思金. 重金属暴露与前列腺癌发生和进展的关系综述[J]. 环境化学, 2014, 33(10): 1776-1783. doi: 10.7524/j.issn.0254-6108.2014.10.015
LI Xiaojian, PAN Dongliang, LI Ningchen, LIU Sijin. Research progression on the effects of heavy metal exposure on prostate cancer[J]. Environmental Chemistry, 2014, 33(10): 1776-1783. doi: 10.7524/j.issn.0254-6108.2014.10.015
Citation: LI Xiaojian, PAN Dongliang, LI Ningchen, LIU Sijin. Research progression on the effects of heavy metal exposure on prostate cancer[J]. Environmental Chemistry, 2014, 33(10): 1776-1783. doi: 10.7524/j.issn.0254-6108.2014.10.015

重金属暴露与前列腺癌发生和进展的关系综述

  • 基金项目:

    环境化学与生态毒理学国家重点实验室开放基金(KF2011-12)资助.

Research progression on the effects of heavy metal exposure on prostate cancer

  • Fund Project:
  • 摘要: 前列腺癌是男性泌尿系统发病率最高的恶性肿瘤.目前关于其发病机制有很多不同的学说,其中环境中的重金属暴露引起前列腺癌的研究逐渐成为研究热点之一.文章重点阐述了镉、砷、铜等重金属导致前列腺癌发生和发展的最新研究进展.研究发现,重金属暴露能够导致前列腺上皮细胞抗凋亡能力增强、雌激素受体增加、DNA甲基化异常、肿瘤干细胞形成,最终导致正常的前列腺上皮细胞发生恶性转化.关于重金属暴露引发前列腺癌的更多机制还有待进一步深入研究.因此,研究环境中重金属暴露导致前列腺癌发生机制对职业性暴露的人群提供健康指导以及预防前列腺癌的发生均具有重要的现实意义.
  • 加载中
  • [1] Siegel R, Ma J, Zou Z, et al. Cancer statistics[J].CA Cancer J Clin, 2014;64:9-29
    [2] 李鸣,张思维,马建辉,等.中国部分市县前列腺癌发病趋势比较研究[J].中华泌尿外科杂,2009,30(6):368-370
    [3] 韩苏军,张思维,陈万青,等.中国前列腺癌发病现状和流行趋势分析[J].临床肿瘤杂志,2013,18(4):330-334
    [4] Akhilesh P, Sharad G, Bhavesh M, et al. Prostate stem cells in the development of benign prostate hyperplasia and prostate cancer: Emerging role and concepts[J].Biomed Res Int, 2013:107954
    [5] Lemen R A, Lee J S, Wagoner J K, et al. Cancer mortality among cadmium production workers[J].Ann NY Acad Sci, 1976, 271:273-279
    [6] Dubrow R, Wegman D H. Cancer and occupation in Massachusetts: A death certificate study[J].Am J Ind Med, 1984, 6(3):207-230
    [7] Elghany N A, Schumacher M C, Slattery M L, et al. Occupation, cadmium exposure, and prostate cancer[J].Epidemiology, 1990, 1(2):107-115
    [8] West DW, Slattery M L, Robison L M, et al. Adult dietary intake and prostate cancer risk in Utah: A case-control study with special emphasis on aggressive tumors[J].Cancer Causes Control, 1991, 2(2):85-94
    [9] IARC. Cadmium and cadmium compounds[J]. IARC Monogr Eval Carcinog Risk Hum.1993, 58:119-237
    [10] Hartwig A. Cadmium and cancer[J].Met Ions Life Sci, 2013, 11:491-507
    [11] Straif K, Brahim-Tallaa L, Baan R, et al. A Review of human carcinogens-part C: Metals, arsenic, fibres, and dusts, and fibres[J].Lancet Oncol, 2009,10(5):453-454
    [12] Aimola P, Carmignani M, Volpe A R, et al. Cadmium induces p53-dependent apoptosis in human prostate epithelial cells[J].PLoS One, 2012, 7(3):e33647
    [13] Achanzar W E, Achanzar K B, Lewis J G, et al. Cadmium induces c-myc, p53, and c-jun expression in normal human prostate epithelial cells as a prelude to apoptosis[J].Toxicol Appl Pharmacol, 2000, 164(3):291-300
    [14] Bakshi S, Zhang X, Godoy-Tundidor S, et al. Transcriptome analyses in normal prostate epithelial cells exposed to low-dose cadmium: Oncogenic and immunomodulations involving the action of tumor necrosis factor[J].Environ Health Perspect, 2008, 116(6):769-776
    [15] Julin B, Wolk A, Johansson J E, et al. Dietary cadmium exposure and prostate cancer incidence: A population-based prospective cohort study[J].Br J Cancer, 2012, 107(5);895-900
    [16] Huff J, Lunn R M, Waalkes M P, et al. Cadmium-induced cancers in animals and in humans[J].Int J Occup Environ Health, 2007,13(2):202-212
    [17] Qu W, Ke H, Pi J, et al. Acquisition of apoptotic resistance in cadmium-transformed human prostate epithelial cells: Bcl-2 overexpression blocks the activation of jnk signal transduction pathway[J].Environ Health Perspect, 2007, 115(7):1094-1100
    [18] Achanzar W E, Webber M M, Waalkes M P. Altered apoptotic gene expression and acquired apoptotic resistance in cadmium-transformed human prostate epithelial cells[J].Prostate, 2002, 52(3):236-244
    [19] Bello D, Webber M M, Kleinman H K, et al. Androgen responsive adult human prostatic epithelial cell lines immortalized by human papillomavirus 18[J].Carcinogenesis, 1997, 18(6): 1215-1223
    [20] Kharbanda S, Saxena S, Yoshida K, et al. Translocation of SAPK/JNK to mitochondria and interaction with Bcl-x(L) in response to DNA damage[J].J Biol Chem, 2000, 275(1): 322-327
    [21] Tournier C, Hess P, Yang D D, et al. Requirement of JNK for stress-induced activation of the cytochrome c-mediated death pathway[J].Science, 2000, 288(5467):870-874
    [22] Vogelstein B, Lane D, Levine A J. Surfing the p53 network[J].Nature. 2000, 408(6810):307-310
    [23] Lag M, Westly S, Lerstad T, et al. Cadmium induced apoptosis of primary epithelial lung cells: Involvement of Bax and p53, but not oxidative stress[J].Cell Biol Toxicol. 2002;18(1): 29-42
    [24] Son Y O, Lee J C, Hitron J A, et al. Cadmium induces intracellular Ca2+ and H2O2-dependent apoptosis through JNK- and P53- mediated pathways in skin epithelial cell line[J].Toxicol Sci, 2010, 113(1):127-137
    [25] Yu X, Sidhu J S, Hong S, et al. Cadmium induced p53-dependent activation of stress signaling, accumulation of ubiquinated proteins, and apoptosis in mouse embryonic fibroblast cells[J].Toxicol Sci, 2011, 120(2):403-412
    [26] Deiry W S, Tokino T, Velculescu V E, et al. WAF1, a potential mediator of p53 tumor suppression[J].Cell, 1993, 75(4): 817-825
    [27] McEleny K R, Watson R W, Coffey R N, et al. Inhibitors of apoptosis proteins in prostate cancer cell lines[J].Prostate, 2002, 51(2):133-140
    [28] Bosland M C. The role of steroid hormones in prostate carcinogenesis[J].J Natl Cancer Inst, 2000, 27:39-66
    [29] Ellem S J, Risbridger G P. Aromatase and regulating the estrogen: Androgen ratio in the prostate gland[J].J Steroid Biochem Mol Biol, 2010, 118(4/5):246-251
    [30] Benbrahim-Tallaa L, Liu J, Webber M M, et al. Estrogen signaling and disruption of androgen metabolism in acquired androgen-independence during cadmium carcinogenesis in human prostate epithelial cells[J].Prostate, 2007, 67(2):135-145
    [31] Stoica A, Katzenellenbogen B S, Martin M B. Activation of estrogen receptor-alpha by the heavy metal cadmium[J].Mol Endocrinol, 2000, 14(4):545-553
    [32] Johnson M D, Kenney N, Stoica A, et al. Cadmium mimics the in vivo effects of estrogen in the uterus and mammary gland[J].Nat Med, 2003, 9(8):1081-1084
    [33] Lai J S, Brown L G, True L D, et al. Metastases of prostate cancer express estrogen receptor-beta[J].Urology, 2004, 64(4):814-820
    [34] Sahlin L. Dexamethasone attenuates the estradiol-induced increase of IGF-1 mRNA in the rat uterus[J].J Steroid Biochem Mol Biol, 1995, 55(1):9-15
    [35] Kaaks R, Lukanova A, Sommersberg B. Plasma androgens, IGF-1, body size, and prostate cancer risk: A synthetic review[J].Prostate Cancer Prostatic Dis, 2000, 3(3):157-172
    [36] Burfeind P, Chernicky C I, Rininsland F, et al. Antisense RNA to the type I insulin-like growth factor receptor suppresses tumor growth and prevents invasion by rat prostate cancer cells in vivo[J].Proc Natl Acad Sci USA, 1996, 93(14):7263-7268
    [37] Bollati V, Baccarelli A. Environmental epigenetics[J].Heredity(Edinb), 2010, 105(1):105-112
    [38] Suganuma T, Workman J L. Crosstalk among Histone Modification[J].Cell, 2008, 135(4):604-607
    [39] Fauque P, Jouannet P, Lesaffre C, et al. Assisted reproductive technology affects developmental kinetics, H19 imprinting control region methylation and H19 gene expression in individual mouse embryos[J].BMC Dev Biol, 2007, 7(1):116
    [40] Ren X, Mchale C M, Skibola C F, et al. An emerging role for epigenetic dysregulation in arsenic toxicity and carcinogenesis[J].Environ Health Perspect, 2011, 119(1):11-19
    [41] Hou L, Zhang X, Wang D, et al. Environmental chemical exposures and human epigenetics[J].Int J Epidemiol, 2012, 41(1):79-105
    [42] Severson P L, Tokar E J, Vrba L, et al. Agglomerates of aberrant DNA methylation are associated with toxicant-induced malignant transformation[J].Epidenetics, 2012, 7(11):1238-1248
    [43] Kristensen L S, Nielsen H M, Hansen L L. Epigenetics and cancer treatment[J].Eur J Pharmacol, 2009, 625(1/3):131-142
    [44] Rauch T, Wang Z, Zhang X, et al. Homeobox gene methylation in lung cancer studied by genome-wide analysis with a microarray-based methylated CpG island recovery assay[J].Proc Natl Acad Sci USA, 2007, 104(13):5527-5532
    [45] Novak P, Jensen T, Oshiro M M, et al. Agglomerative epigenetic aberrations are a common event in human breast cancer[J].Cancer Res, 2008, 68(20):8616-8625
    [46] Novak P, Jensen T, Oshiro M M, et al. Epigenetic inactivation of the HOXA gene cluster in breast cancer[J].Cancer Res, 2006, 66(22):10664-10670
    [47] Coolen M W, Stirzaker C, Song J Z, et al. Consolidation of the cancer genome into domains of repressive chromatin by long-range epigenetic silencing(LRES) reduces transcriptional plasticity[J].Nat Cell Biol, 2010, 12(3):235-246
    [48] IARC. Some drinking-water disinfectants and contaminants, including arsenic. IARC Monogr Eval Carcinog Risks Hum[J].2004, 84:269-477
    [49] Ferreccio C, Smith A H, Duran V, et al. Case-control study of arsenic in drinking water and kidney cancer in uniquely exposed northern Chile[J].Am J Epidemiol,2013, 178(5):813-818
    [50] Garcia-Esquinas E, Pollan M, Umans J G, et al. Arsenic exposure and cancer mortality in a US-based prospective cohort: The strong heart study[J].Cancer Epidemiol Biomarkers Prev, 2013, 22(11):1944-1953
    [51] Benbrahim-Tallaa L, Waalkes M P. Inorganic arsenic and human prostate cancer[J].Environ Health Perspect, 2008, 116(2):158-164
    [52] Yang C Y, Chang C C, Chiu H F. Dose arsenic exposure increase the risk for prostate cancer?[J].J Toxicol Environ Health A, 2008, 71(23):1559-1563
    [53] Wallace D C. Mitochondrial diseases in man and mouse[J].Science, 1999, 283(5407):1482-1488
    [54] Barchosky A, Klei L R, Dudek E J, et al. Stimulation of reactive oxygen, but not reactive nitrogen species, in vascular endothelial cells exposed to low levels of arsenite[J].Free Radical Biol Med, 1999, 27(11/12):1405-1412
    [55] Liu S X, Athar M, Lippai I, et al. Induction of oxyradicals by arsenic: Implication for mechanism of genotoxicity[J].Proc Natl Acad Sci USA, 2001, 98(4):1643-1648
    [56] Singh K P, Kumari R, Treas J, et al. Chronic exposure to arsenic causes increased cell survival, DNA damage, and increased expression of mitochondrial transcription factor A(mtTFA) in human prostate epithelial cells[J].Chem Res Toxicol, 2011, 24(3):340-349
    [57] Jaenisch R, Bird A. Epigenetic regulation of gene expression: How the genome integrates intrinsic and environmental signals[J].Nat Genet, 2003, 33:245-254
    [58] Laird P W, Jaenisch R. DNA methylation and cancer[J].Hum Mol Genet, 1994, 3:1487-1495
    [59] Benbrahim-Tallaa L, Waterland R A, Styblo M, et al. Molecular events associated with arsenic-induced malignant transformation of human prostatic epithelial cells: Aberrant genomic DNA methylation and K-ras oncogene activation[J].Toxicol Appl Pharmacol, 2005, 206(3):288-298
    [60] Iqbal J, Chong P Y, Tan P H. Breast cancer stem cells: An update[J].J Clin Pathol, 2013, 66(6):485-490
    [61] Ricci-vitian L, Lombardi D G, Pilozzi E, et al. Identification and expansion of human colon-cancer-initiating cells[J].Nature, 2007, 445(7123):111-115
    [62] Li C, Heidt D G, Dalerba P, et al. Identification of pancreatic cancer stem cells[J].Cancer Res, 2007, 67(3):1030-1037
    [63] Lee T K, Castilho A, Cheung V C, et al. CD24+ liver tumor-initiating cells drive self-renewal and tumor initiation through STAT3-mediated NANOG regulation[J].Cell Stem Cell, 2011, 9(1):50-63
    [64] Curtis S J, Sinkevivius K W, Li D, et al. Primary tumor genotype is an important determinant in identification of lung cancer propagating cells[J].Cell Stem Cell, 2010, 7(1):127-133
    [65] Tokar E J, Diwan B A, Waalkes M P, et al. Arsenic exposure transforms human epithelial stem/progenitor cells into a cancer stem-like phenotype[J].Environ Health Perspect, 2010, 118(1):108-115
    [66] Xu Y, Tokar E J, Sun Y, et al. Arsenic-transformed malignant prostate epithelia can convert noncontiguous normal stem cells into an oncogenic phenotype[J].Environ Health Perspect, 2012, 120(6):865-871
    [67] Tisato F, Marzano C, Porcbia M, et al. Copper in diseases and treatments, and copper-based anticancer strategies[J].Med Res Rev, 2010, 30(4):708-749
    [68] Karimi G, Shahar S, Homayouni N, et al. Association between trace element and heavy metal levels in hair and nail with prostate cancer[J].Asian Pac J Cancer Prev, 2012, 13(9):4249-4253
    [69] Hayashida K, Bartlett A H, Chen Y, et al. Molecular and cellular mechanisms of ectodomain shedding[J].Anat Rec(Hoboken), 2010, 293(6):925-937
    [70] Duffy M J, Mullooly M, O'Donovan N, et al. The ADAMs family of proteases: New biomarkers and therapeutic targets for cancer?[J].Clin Proteomics, 2011, 8(1):9
    [71] Hua H, Li M, Luo T, et al. Matrix metalloproteinases in tumorigenesis: An evolving paradigm[J].Cell Mol Life Sci, 2011, 68(23):3853-3868
    [72] Parr-Sturgess C A, Tinker C L, Hart C A, et al. Copper modulates zinc metalloproteinase-dependent ectodomain shedding of key signaling and adhesion proteins and promotes the invasion of prostate cancer epithelial cells[J].Mol Cancer Res, 2012, 10(10):1282-1293
    [73] Ozmen H, Erulas F A, Karatas F, et al. Comparison of the concentration of trace metals (Ni, Zn, Co, Cu and Se), Fe, vitamins A, C and E, and lipid peroxidation in patients with prostate cancer[J].Clin Chem Lab Med, 2006, 44(2):175-179
    [74] Lu N, Zhou H, Lin Y H, et al. Oxidative stress mediates CoCl(2)-induced prostate tumour cell adhesion: role of protein kinase C and p38 mitogen-activated protein kinase[J].Basic Clin Pharmacol Toxicol, 2007, 101(1):41-46
    [75] Tsui K H, Chang P L, Juang H H. Manganese antagonizes iron blocking mitochondrial aconitase expression in human prostate carcinoma cells[J].Asian J Androl, 2006, 8(3):307-315
    [76] Yaman M, Atici D, Bakirdere S, et al. Comparison of trace metal concentrations in malign and benign human prostate[J].J Med Chem, 2005, 48(2):630-634
  • 加载中
计量
  • 文章访问数:  2145
  • HTML全文浏览数:  2145
  • PDF下载数:  847
  • 施引文献:  0
出版历程
  • 收稿日期:  2014-06-16
李晓建, 潘东亮, 李宁忱, 刘思金. 重金属暴露与前列腺癌发生和进展的关系综述[J]. 环境化学, 2014, 33(10): 1776-1783. doi: 10.7524/j.issn.0254-6108.2014.10.015
引用本文: 李晓建, 潘东亮, 李宁忱, 刘思金. 重金属暴露与前列腺癌发生和进展的关系综述[J]. 环境化学, 2014, 33(10): 1776-1783. doi: 10.7524/j.issn.0254-6108.2014.10.015
LI Xiaojian, PAN Dongliang, LI Ningchen, LIU Sijin. Research progression on the effects of heavy metal exposure on prostate cancer[J]. Environmental Chemistry, 2014, 33(10): 1776-1783. doi: 10.7524/j.issn.0254-6108.2014.10.015
Citation: LI Xiaojian, PAN Dongliang, LI Ningchen, LIU Sijin. Research progression on the effects of heavy metal exposure on prostate cancer[J]. Environmental Chemistry, 2014, 33(10): 1776-1783. doi: 10.7524/j.issn.0254-6108.2014.10.015

重金属暴露与前列腺癌发生和进展的关系综述

  • 1.  北京大学首钢医院泌尿外科, 北京, 100144;
  • 2.  中国科学院生态环境研究中心, 北京, 100085
基金项目:

环境化学与生态毒理学国家重点实验室开放基金(KF2011-12)资助.

摘要: 前列腺癌是男性泌尿系统发病率最高的恶性肿瘤.目前关于其发病机制有很多不同的学说,其中环境中的重金属暴露引起前列腺癌的研究逐渐成为研究热点之一.文章重点阐述了镉、砷、铜等重金属导致前列腺癌发生和发展的最新研究进展.研究发现,重金属暴露能够导致前列腺上皮细胞抗凋亡能力增强、雌激素受体增加、DNA甲基化异常、肿瘤干细胞形成,最终导致正常的前列腺上皮细胞发生恶性转化.关于重金属暴露引发前列腺癌的更多机制还有待进一步深入研究.因此,研究环境中重金属暴露导致前列腺癌发生机制对职业性暴露的人群提供健康指导以及预防前列腺癌的发生均具有重要的现实意义.

English Abstract

参考文献 (76)

返回顶部

目录

/

返回文章
返回