Meme Kanseri Epigenetiğinde Biyobelirteçler: Çevresel Faktörlerin Etkisi

Ela Tuğrul Karataş; Muhammet Osman Karataş; Sibel Özden

doi:10.52794/hujpharm.1424049

TR EN

Meme Kanseri Epigenetiğinde Biyobelirteçler: Çevresel Faktörlerin Etkisi

Abstract

Meme kanseri, dünya çapında kadınlardaki kansere bağlı ölümlerin başlıca nedenlerinden biridir. Meme kanseri hormonal, genetik, yaşam tarzı gibi birçok risk faktörü ile ilişkilendirilmiştir. Ancak günümüzde artan kanıtlar çevresel kirleticilere maruziyetin meme kanseri gelişiminde göz ardı edilemez bir risk faktörü olduğunu ortaya koymaktadır. Özellikle, bazı çevresel kirleticiler; DNA metilasyonu, histon modifikasyonu ve mikroRNA (miRNA)’ lardaki değişiklikler gibi epigenetik mekanizmalarla gen ifadesini değiştirebilir. Çevresel kirleticilere bağlı bu modifikasyonlarda saptanan epigenetik biyobelirteçlerin, meme kanserinde erken teşhis ve prognozun belirlenmesinde anahtar olabileceği düşünülmektedir. Günümüzde miRNA’lar meme kanseri araştırmalarında yeni biyobelirteçler olarak kullanılmaktadır. Doku, tam kan, serum ve plazmadan izole edilebilmesi ve biyobelirteç olarak kullanım kolaylığı miRNA’ları önemli bir teşhis aracı haline getirmiştir. Bu derlemenin çevresel kirleticilere maruziyet sonucu değişiklik gözlenen epigenetik biyobelirteçler ile meme kanseri riski arasındaki ilişkiye ışık tutacağı düşünülmektedir. Bu derlemede aril hidrokarbon reseptör agonistleri (dioksinler, poliklorlu bifeniller, polisiklik aromatik hidrokarbonlar), ftalatlar, bisfenol A ve arsenik gibi çevresel kirleticilerin epigenetik mekanizmalardaki etkisine odaklanılmıştır. Meme kanseri vakalarında epigenetik araştırmaların artması ile çevresel maruziyetlerin azalacağı ve kişiselleştirilmiş önleyici stratejilerin geliştirilebileceği düşünülmektedir.

Keywords

Biomarkers in Breast Cancer Epigenetics: Effect of Environmental Factors

Abstract

Breast cancer is one of the leading causes of cancer-related deaths in women worldwide. Breast cancer has been associated with many risk factors like hormonal, genetics and lifestyle. However, emerging evidence highlights the significant role of environmental pollutants as a risk factor in breast cancer development. Especially some environmental pollutants can change gene expression through epigenetic mechanisms like DNA methylation, histone modification and micro-RNA changes. Epigenetic biomarkers from environmental pollutants may aid early diagnosis and prognosis in breast cancer. Nowadays, microRNAs are used as new biomarkers in breast cancer research. The ability to isolate from tissue, whole blood, serum and plasma and the ease of use as a biomarker has made miRNAs an important diagnostic tool. This review aims to shed light on the relationship between epigenetic biomarkers observed to change due to exposure to environmental pollutants and the risk of breast cancer. In this review the effects of environmental pollutants such as aryl hydrocarbon receptor agonists (dioxins, polychlorinated biphenyls, polycyclic aromatic hydrocarbons), phthalates, bisphenol A, and arsenic on epigenetic mechanisms is focused. It is thought that environmental exposures will decrease and personalized preventive strategies can be developed with the increase in epigenetic researches in breast cancer cases.

Keywords

References

1. Moslehi R, Freedman E, Zeinomar N, Veneroso C, Levine PH. Importance of hereditary and selected environmental risk factors in the etiology of inflammatory breast cancer: a case-comparison study. BMC Canc. 2016;16:334. https://doi.org/10.1186/s12885-016-2369-z
2. Knower KC, To SQ, Leung YK, Ho SM, Clyne CD. Endocrine disruption of the epigenome: a breast cancer link. Endocr Relat Cancer. 2014;21(2):T33-T55. https://doi.org/10.1530/ERC-13-0513
3. Moslehi R, Stagnar C, Srinivasan S, Radziszowski P, Carpenter DO. The possible role of arsenic and gene-arsenic interactions in susceptibility to breast cancer: a systematic review. Rev Environ Health. 2021;36(4):523-534. https://doi.org/10.1515/reveh-2020-0080
4. Park HL. Epigenetic biomarkers for environmental exposures and personalized breast cancer prevention. Int J Environ Res Public Health. 2020;17(4):1181. https://doi.org/10.3390/ijerph17041181
5. Buocikova V, Rios-Mondragon I, Pilalis E, Chatziioannou A, Miklikova S, Mego M, et al. Epigenetics in breast cancer therapy—New strategies and future nanomedicine perspectives. Cancers. 2020;12(12):3622. https://doi.org/10.3390/cancers12123622
6. Sharavanan VJ, Sivaramakrishnan M, Sivarajasekar N, Senthilrani N, Kothandan R, Dhakal N, et al. Pollutants inducing epigenetic changes and diseases. Environ Chem Lett. 2020;18:325-343. https://doi.org/10.1007/s10311-01900944-3
7. Thakur C, Qiu Y, Fu Y, Bi Z, Zhang W, Ji H, et al. Epigenetics and environment in breast cancer: New paradigms for anticancer therapies. Front Oncol. 2022;12:971288. https://doi.org/10.3389/fonc.2022.971288
8. Evron E, Dooley WC, Umbricht CB, Rosenthal D, Sacchi N, Gabrielson E, et al. Detection of breast cancer cells in ductal lavage fluid by methylation specific PCR. Lancet. 2001;357(9265):1335–1336. https://doi.org/10.1016/S01406736(00)045013

9. Krassenstein R, Sauter E, Dulaimi E, Battagli C, Ehya H, Klein-Szanto A, et al. Detection of breast cancer in nipple aspirate fluid by CpG island hypermethylation. Clin Cancer Res. 2004;10(1):28–32. https://doi.org/10.1158/1078-0432.ccr0410-3
10. Silva JM, Garcia JM, Dominguez G, Silva J, Miralles C, Cantos B, et al. Persistence of tumor DNA in plasma of breast cancer patients after mastectomy. Ann Surg Oncol. 2002;9(1):71–76. https://doi.org/10.1245/aso.2002.9.1.71
11. Dulaimi E, Hillinck J, de Caceres II, Al-Saleem T, Cairns P. Tumor suppressor gene promoter hypermethylation in serum of breast cancer patients. Clin Cancer Res. 2004;10(18): 6189–6193. https://doi.org/10.1158/1078-0432.CCR-04-0597
12. Kapoor-Vazirani P, Kagey JD, Powell DR, Vertino PM. Role of hMOF-dependent histone H4 lysine 16 acetylation in the maintenance of TMS1/ASC gene activity. Cancer Res. 2008;68(16):6810-6821. https://doi.org/10.1158/0008-5472.CAN-08-0141
13. Yang X, Karuturi RM, Sun F, Aau M, Yu K, Shao R, et al. CDKN1C (p57) is a direct target of EZH2 and suppressed by multiple epigenetic mechanisms in breast cancer cells. PLoS One. 2009;4(4):e5011. https://doi.org/10.1371/journal.pone.0005011
14. Christodoulatos GS, Dalamaga M. Micro-RNAs as clinical bi- omarkers and therapeutic targets in breast cancer: quo vadis?. World J Clin Oncol. 2014;5(2):71–81. https://doi.org/10.5306/wjco.v5.i2.71
15. Mattiske S, Suetani RJ, Neilsen PM, Callen DF. The oncogenic role of miR-155 in breast cancer. Cancer Epidemiol Biomarkers Prev. 2012;21(8):1236-1243. https://doi.org/10.1158/1055-9965.EPI-120173
16. Corcoran C, Friel AM, Duffy MJ, Crown J, O’Driscoll L. Intracellular and extracellular microRNAs in breast cancer. Clin Chem. 2011;57(1):18-32. https://doi.org/10.1373/clinc-hem.2010.150730
17. Zhang H, Cai K, Wang J, Wang X, Cheng K, Shi F, et al. MiR-7, inhibited indirectly by lincRNA HOTAIR, directly inhibits SETDB1 and reverses the EMT of breast cancer stem cells by downregulating the STAT3 pathway. Stem Cells. 2014;32(11):2858–2868. https://doi.org/10.1002/stem.1795
18. Yu N, Huangyang P, Yang X, Han X, Yan R, Jia H, et al. MicroRNA-7 suppresses the invasive potential of breast cancer cells and sensitizes cells to DNA damages by targeting histone methyltransferase SET8. J Biol Chem. 2013;288(27):19633–19642. https://doi.org/10.1074/jbc.M113.475657
19. Ahmad A, Ginnebaugh KR, Yin S, Bollig-Fischer A, Reddy KB, Sarkar FH. Functional role of miR-10b in tamoxifen resistance of ER-positive breast cancer cells through down- regulation of HDAC4. BMC Cancer. 2015;15(1):540. https://doi.org/10.1186/s12885-015-1561-x
20. Ma L, Teruya-Feldstein J, Weinberg RA. Tumour invasion and metastasis initiated by microRNA-10b in breast cancer. Nature. 2007;449(7163):682–688. https://doi.org/10.1038/nature06174
21. Ao X, Nie P, Wu B, Xu W, Zhang T, Wang S, et al. Decreased expression of microRNA-17 and microRNA-20b promotes breast cancer resistance to taxol therapy by upregulation of NCOA3. Cell Death Dis. 2016;7(11):e2463. https://doi.org/10.1038/cddis.2016.367
22. Hossain A, Kuo MT, Saunders GF. Mir-17-5p regulates breast cancer cell proliferation by inhibiting translation of AIB1 mRNA. Mol Cell Biol. 2006;26(21):8191–8201. https://doi.org/10.1128/MCB.00242-06
23. Zhu S, Si ML, Wu H, Mo YY. MicroRNA-21 targets the tumor suppressor gene tropomyosin 1 (TPM1). J Biol Chem. 2007;282(19):14328–14336. https://doi.org/10.1074/jbc.M611393200
24. Frankel LB, Christoffersen NR, Jacobsen A, Lindow M, Krogh A, Lund AH. Programmed cell death 4 (PDCD4) is an important functional target of the microRNA miR-21 in breast cancer cells. J Biol Chem. 2008;283(2):1026–1033. https://doi.org/10.1074/jbc.M707224200
25. Qi L, Bart J, Tan LP, Platteel I, Sluis Tvd, Huitema S, et al. Expression of miR-21 and its targets (PTEN, PDCD4, TM1) in flat epithelial atypia of the breast in relation to ductal carcinoma in situ and invasive carcinoma. BMC Cancer. 2009;9:163. https://doi.org/10.1186/1471-2407-9-163
26. Wang B, Li D, Filkowski J, Rodriguez-Juarez R, Storozynsky Q, Malach M, et al. A dual role of miR-22 modulated by RelA/ p65 in resensitizing fulvestrant-resistant breast cancer cells to fulvestrant by targeting FOXP1 and HDAC4 and constitutive acetylation of p53 at Lys382. Oncogenesis. 2018;7(7):54. https://doi.org/10.1038/s41389-018-0063-5
27. Pandey P, Zhang Y, Zhang S, Li Y, Tucker-Kellog G, Yang H, et al. TIP60-miR-22 axis as a prognostic marker of breast cancer progression. Oncotarget. 2015;6(38):41290–41306. https://doi.org/10.18632/oncotarget.5636
28. Song SJ, Poliseno L, Song MS, Ala U, Webster K, Ng C, et al. MicroRNA-antagonism regulates breast cancer stemness and metastasis via TET-family-dependent chromatin remodeling. Cell. 2013;154(2):311–324. https://doi.org/10.1016/j.cell.2013.06.026
29. Shao P, Liu Q, Maina PK, Cui J, Bair TB, Li T, et al. Histone demethylase PHF8 promotes epithelial to mesenchymal transition and breast tumorigenesis. Nucleic Acids Res. 2017;45(4):1687–1702. https://doi.org/10.1093/nar/gkw1093
30. Zhou Y, Hu Y, Yang M, Jat P, Li K, Lombardo Y, et al. The miR-106b~25 cluster promotes bypass of doxorubicin-induced senescence and increase in motility and invasion by targeting the E-cadherin transcriptional activator EP300. Cell Death Differ. 2014;21(3):462–474. https://doi.org/10.1038/cdd.2013.167
31. Zhang B, Liu XX, He JR, Zhou CX, Guo M, He M, et al. Pathologically decreased miR-26a antagonizes apoptosis and facilitates carcinogenesis by targeting MTDH and EZH2 in breast cancer. Carcinogenesis. 2011;32(1):2–9. https://doi.org/10.1093/carcin/bgq209
32. Pei YF, Lei Y, Liu XQ. MiR-29a promotes cell proliferation and EMT in breast cancer by targeting ten eleven translocation 1. Biochim. Biophys. Acta. 2016;1862(11):2177–2185. https://doi.org/10.1016/j.bbadis.2016.08.014
33. Valastyan S, Reinhardt F, Benaich N, Calogrias D, Szász AM, Wang ZC, et al. A pleiotropically acting microRNA, miR-31, inhibits breast cancer metastasis. Cell. 2009;137(6):1032–1046. https://doi.org/10.1016/j.cell.2009.03.047
34. Wu MY, Fu J, Xiao X, Wu J, Wu RC. MiR-34a regulates therapy resistance by targeting HDAC1 and HDAC7 in breast cancer. Cancer Lett. 2014;354(2):311–319. https://doi.org/10.1016/j.canlet.2014.08.031
35. O’Day E, Lal A. MicroRNAs and their target gene networks in breast cancer. Breast Cancer Res. 2010;12(2):201. https://doi.org/10.1186/bcr2484
36. Ma W, Xiao GG, Mao J, Lu Y, Song B, Wang L, et al. Dysregulation of the miR-34a-SIRT1 axis inhibits breast cancer stemness. Oncotarget. 2015;6(12):10432–10444. https://doi.org/10.18632/oncotarget.3394
37. Liu F, Sang M, Meng L, Gu L, Liu S, Li J, et al. MiR92b promotes autophagy and suppresses viability and invasion in breast cancer by targeting EZH2. Int J Oncol. 2018;53(4):1505-1515. https://doi.org/10.3892/ijo.2018.4486
38. Varambally S, Cao Q, Mani RS, Shankar S, Wang X, Ateeq B, et al. Genomic Loss of microRNA-101 Leads to Overexpression of Histone Methyltransferase EZH2 in Cancer. Science. 2008;322(5908):1695–1699. https://doi.org/10.1126/science.1165395
39. Hsieh TH, Hsu CY, Tsai CF, Long CY, Chai CY, Hou MF, et al. MiR-125a-5p is a prognostic biomarker that targets HDAC4 to suppress breast tumorigenesis. Oncotarget. 2014;6(1):494–509. https://doi.org/10.18632/oncotarget.2674
40. Adlakha YK, Saini N. miR-128 exerts pro-apoptotic effect in a p53 transcription-dependent and -independent manner via PUMA-Bak axis. Cell Death Dis. 2013;4(3):e542. https://doi.org/10.1038/cddis.2013.46
41. Eedunuri VK, Rajapakshe K, Fiskus W, Geng C, Chew SA, Foley C, et al. miR-137 Targets p160 Steroid Receptor Co-activators SRC1, SRC2, and SRC3 and Inhibits Cell Proliferation. Mol Endocrinol. 2015;29(8):1170–1183. https://doi.org/10.1210/me.2015-1080
42. Wang K, Yang F, Men X, Li G, Sun C. MiR-138 suppresses EMT through degradation KDM6B in breast carcinoma. Int J Clin Exp Med. 2016;9:4724–4733.
43. Ng EK, Li R, Shin VY, Siu JM, Ma ES, Kwong A. MicroRNA-143 is downregulated in breast cancer and regulates DNA methyltransferases 3A in breast cancer cells. Tumour Biol. 2014;35(3):2591–2598. https://doi.org/10.1007/s13277-013-1341-7
44. Elhelbawy NG, Zaid IF, Khalifa AA, Gohar SF, Fouda EA. miRNA-148a and miRNA-30c expressions as potential biomarkers in breast cancer patients. Biochem Biophys Rep. 2021;27:101060. https://doi.org/10.1016/j.bbrep.2021.101060
45. Xu Q, Jiang Y, Yin Y, Li Q, He J, Jing Y, et al. A regulatory circuit of miR-148a/152 and DNMT1 in modulating cell transformation and tumor angiogenesis through IGF-IR and IRS1. J Mol Cell Biol. 2013;5(1):3–13. https://doi.org/10.1093/jmcb/mjs049
46. Kong W, Yang H, He L, Zhao J-j, Coppola D, Dalton WS, et al. MicroRNA-155 is regulated by the transforming growth factor beta/Smad pathway and contributes to epithelial cell plasticity by targeting RhoA. Mol Cell Biol. 2008;28(22):6773–6784. https://doi.org/10.1128/MCB.00941-08
47. Tang H, Liu P, Yang L, Xie X, Ye F, Wu M, et al. miR-185 suppresses tumor proliferation by directly targeting E2F6 and DNMT1 and indirectly upregulating BRCA1 in triple-negative breast cancer. Mol Cancer Ther. 2014;13(12):3185–3197. https://doi.org/10.1158/1535-7163.MCT-14-0243
48. Derfoul A, Juan AH, Difilippantonio MJ, Palanisamy N, Ried T, Sartorelli V. Decreased microRNA-214 levels in breast cancer cells coincides with increased cell proliferation, invasion and accumulation of the Polycomb Ezh2 methyltransferase. Carcinogenesis. 2011;32(11):1607–1614. https://doi.org/10.1093/carcin/bgr184
49. Eades G, Yao Y, Yang M, Zhang Y, Chumsri S, Zhou Q. miR- 200a regulates SIRT1 expression and epithelial to mesenchymal transition (EMT)-like transformation in mammary epithelial cells. J Biol Chem. 2011;286(29):25992–26002. https://doi.org/10.1074/jbc.M111.229401
50. Pang Y, Liu J, Li X, Xiao G, Wang H, Yang G, et al. MYC and DNMT3A-mediated DNA methylation represses microRNA-200b in triple negative breast cancer. J Cell Mol Med. 2018;22(12):6262–6274. https://doi.org/10.1111/jcmm.13916
51. Iliopoulos D, Lindahl-Allen M, Polytarchou C, Hirsch HA, Tsichlis PN, Struhl K. Loss of miR-200 inhibition of Suz12 leads to polycomb-mediated repression required for the formation and maintenance of cancer stem cells. Mol Cell. 2010;39(5):761–772. https://doi.org/10.1016/j.molcel.2010.08.013
52. Adams BD, Furneaux H, White BA. The micro-ribonucleic acid (miRNA) miR-206 targets the human estrogen receptor- alpha (ERalpha) and represses ERalpha messenger RNA and protein expression in breast cancer cell lines. Mol Endocri- nol. 2007;21(5):1132–1147. https://doi.org/10.1210/me.2007-0022
53. Chen LL, Zhang ZJ, Yi ZB, Li JJ. MicroRNA-211-5p suppresses tumour cell proliferation, invasion, migration and metastasis in triple-negative breast cancer by directly targeting SETBP1. Br J Cancer. 2017;117(1):78–88. https://doi.org/10.1038/bjc.2017.150
54. Roscigno G, Quintavalle C, Donnarumma E, Puoti I, Di- az-Lagares A, Iaboni M, et al. Mir-221 promotes stemness of breast cancer cells by targeting DNMT3b. Oncotarget. 2015;7(1):580–592. https://doi.org/10.18632/oncotarget.5979
55. Shi Z, Li Y, Qian X, Hu Y, Liu J, Zhang S, et al. MiR-340 Inhibits Triple-Negative Breast Cancer Progression by Reversing EZH2 Mediated miRNAs Dysregulated Expressions. J Cancer. 2017;8(15):3037–3048. https://doi.org/10.7150/jca.19315
56. Weng C, Nguyen T, Shively JE. miRNA-342 Regulates CEACAM1-induced Lumen Formation in a Three-dimensional Model of Mammary Gland Morphogenesis. J Biol Chem. 2016;291(32):16777–16786. https://doi.org/10.1074/jbc.M115.710152
57. Huang Q, Gumireddy K, Schrier M, le Sage C, Nagel R, Nair S, et al. The microRNAs miR-373 and miR-520c promote tumour invasion and metastasis. Nat Cell Biol. 2008;10(2):202-210. https://doi.org/10.1038/ncb1681
58. Wu M, Fan B, Guo Q, Li Y, Chen R, Lv N, et al. Knockdown of SETDB1 inhibits breast cancer progression by miR-381-3p-related regulation. Biol Res. 2018;51(1):39. https://doi.org/10.1186/s40659-018-0189-0
59. Bamodu OA, Huang WC, Lee WH, Wu A, Wang LS, Hsiao M, et al. Aberrant KDM5B expression promotes aggressive breast cancer through MALAT1 overexpression and downregulation of hsa-miR-448. BMC Cancer. 2016;16(1):160. https://doi.org/10.1186/s12885-016-2108-5
60. Romagnolo DF, Daniels KD, Grunwald JT, Ramos SA, Propper CR, Selmin OI. Epigenetics of breast cancer: Modifying role of environmental and bioactive food compounds. Mol Nutr Food Res. 2016;60(6):1310-1329. https://doi.org/10.1002/mnfr.201501063
61. Sweeney C, Lazennec G, Vogel CF. Environmental exposure and the role of AhR in the tumor microenvironment of breast cancer. Front Pharmacol. 2022;13:1095289. https://doi.org/10.3389/fphar.2022.1095289
62. Eltom SE, Gasmelseed AA, Saoudi-Guentri D. The aryl hydrocarbon receptor is over-expressed and constitutively activated in advanced breast carcinoma. Cancer Res. 2006;66(8_Supp- lement):408.
63. Schlezinger JJ, Liu D, Farago M, Seldin DC, Belguise K, Sonenshein GE, et al. A role for the aryl hydrocarbon receptor in mammary gland tumorigenesis. Biol Chem. 2006;387(9):1175- 1187. https://doi.org/10.1515/BC.2006.145
64. Del Pup L, Mantovani A, Cavaliere C, Facchini G, Luce A, Sperlongano P, et al. Carcinogenetic mechanisms of endocrine disruptors in female cancers. Oncol Rep. 2016;36(2):603-612. https://doi.org/10.3892/or.2016.4886
65. Tsuchiya Y, Nakajima M, Takagi S, Taniya T, Yokoi T. MicroRNA regulates the expression of human cytochrome P450 1B1. Cancer Res. 2006;66(18):9090-9098. https://doi.org/10.1158/0008-5472.CAN-06-1403
66. Papoutsis AJ, Borg JL, Selmin OI, Romagnolo DF. BRCA-1 promoter hypermethylation and silencing induced by the aromatic hydrocarbon receptor-ligand TCDD are prevented by resveratrol in MCF-7 cells. J Nutr Biochem. 2012;23(10):1324-1332. https://doi.org/10.1016/j.jnutbio.2011.08.001
67. Beedanagari SR, Taylor RT, Bui P, Wang F, Nickerson DW, Hankinson O. Role of epigenetic mechanisms in differential regulation of the dioxin-inducible human CYP1A1 and CYP1B1 genes. Mol Pharmacol. 2010;78(4):608-616. https://doi.org/10.1124/mol.110.064899
68. Donovan MG, Selmin OI, Romagnolo DF. Focus: Nutrition and Food Science: Aryl Hydrocarbon Receptor Diet and Breast Cancer Risk. Yale J Biol Med. 2018;91(2):105-127.
69. Jeffy BD, Chirnomas RB, Romagnolo DF. Epigenetics of breast cancer: polycyclic aromatic hydrocarbons as risk factors. Environ Mol Mutagen. 2002;39(2-3):235-244. https://doi.org/10.1002/em.10051
70. Romagnolo DF, Papoutsis AJ, Laukaitis C, Selmin OI. Constitutive expression of AhR and BRCA-1 promoter CpG hypermethylation as biomarkers of ERα-negative breast tumorigenesis. BMC Cancer. 2015;15:1026. https://doi.org/10.1186/s12885-015-2044-9
71. Miret NV, Pontillo CA, Buján S, Chiappini FA, Randi AS. Mechanisms Of Breast Cancer Progression Induced BY Environment-Polluting ARYL Hydrocarbon Receptor Agonists. Biochem Pharmacol. 2023;216:115773. https://doi.org/10.1016/j.bcp.2023.115773
72. Sahay D, Terry MB, Miller R. Is breast cancer a result of epigenetic responses to traffic-related air pollution? A review of the latest evidence. Epigenomics. 2019;11(6):701-714. https://doi.org/10.2217/epi-2018-0158
73. Singh S, Li SSL. Epigenetic effects of environmental chemicals bisphenol A and phthalates. Int J Mol Sci. 2012;13(8):10143-10153. https://doi.org/10.3390/ijms130810143
74. Böckers M, Paul NW, Efferth T. Butyl octyl phthalate interacts with estrogen receptor α in MCF7 breast cancer cells to promote cancer development. World Acad Sci J. 2021;3(2): 1-1. https://doi.org/10.3892/wasj.2021.92
75. Deb P, Bhan A, Hussain I, Ansari KI, Bobzean SA, Pandita TK, et al. Endocrine disrupting chemical, bisphenol-A, induces breast cancer associated gene HOXB9 expression in vitro and in vivo. Gene. 2016;590(2):234-243. https://doi.org/10.1016/j.gene.2016.05.009
76. Bhan A, Hussain I, Ansari KI, Bobzean SA, Perrotti LI, Mandal SS. Histone methyltransferase EZH2 is transcriptionally induced by estradiol as well as estrogenic endocrine disruptors bisphenol-A and diethylstilbestrol. J Mol Biol. 2014;426(20):3426-3441. https://doi.org/10.1016/j.jmb.2014.07.025
77. Bhan A, Hussain I, Ansari KI, Bobzean SA, Perrotti LI, Mandal SS. Bisphenol-A and diethylstilbestrol exposure induces the expression of breast cancer associated long noncoding RNA HOTAIR in vitro and in vivo. J Steroid Biochem Mol Biol. 2014;141:160-170. https://doi.org/10.1016/j.jsbmb.2014.02.002
78. Orloff K, Mistry K, Metcalf S. Biomonitoring for environmental exposures to arsenic. J Toxicol Environ Health B Crit Rev. 2009;12(7):509-524. https://doi.org/10.1080/10937400903358934
79. Straif K, Benbrahim-Tallaa L, Baan R, Grosse Y, Secretan B, El Ghissassi F, et al. A review of human carcinogens–Part C: metals, arsenic, dusts, and fibres. Lancet Oncol. 2009;10(5): 453–454. https://doi.org/10.1016/s1470-2045(09)70134-2
80. Smeester L, Rager JE, Bailey KA, Guan X, Smith N, Garcia- Vargas G, et al. Epigenetic changes in individuals with arsenicosis. Chem Res Toxicol. 2011;24(2):165–167. https://doi.org/10.1021/tx1004419
81. Chen QY, DesMarais T, Costa M. Metals and mechanisms of carcinogenesis. Annu Rev Pharmacol Toxicol. 2019;59:537–554. https://doi.org/10.1146/annurev-pharmtox-010818-021031
82. Wu K, Li L, Thakur C, Lu Y, Zhang X, Yi Z, et al. Proteomic characterization of the world trade center dust-activated mdig and c-myc signaling circuit linked to multiple myeloma. Sci Rep. 2016;6(1):36305. https://doi.org/10.1038/srep36305
83. Zhang Y, Lu Y, Yuan BZ, Castranova V, Shi X, Stauffer JL, et al. The human mineral dust-induced gene, mdig, is a cell growth regulating gene associated with lung cancer. Oncogene. 2005;24(31):4873–4882. https://doi.org/10.1038/sj.onc.1208668
84. Zhang Q, Thakur C, Shi J, Sun J, Fu Y, Stemmer P, et al. New discoveries of mdig in the epigenetic regulation of cancers. Semin Cancer Biol. 2019;57:27–35. https://doi.org/10.1016/j.semcancer.2019.06.013
85. Cos P, De Bruyne T, Apers S, Vanden Berghe D, Pieters L, Vlietinck AJ. Phytoestrogens: recent developments. Planta Med. 2003;69(7):589–599. https://doi.org/10.1055/s-2003-41122
86. Maggiolini M, Bonofiglio D, Marsico S, Panno ML, Cenni B, Picard D, et al. Estrogen receptor α mediates the proliferative but not the cytotoxic dose-dependent effects of two major phytoestrogens on human breast cancer cells. Mol Pharmacol. 2001;60(3):595–602.
87. Trock BJ, Hilakivi-Clarke L, Clarke R. Meta-analysis of soy intake and breast cancer risk. J Natl Cancer Inst. 2006;98(7):459–471. https://doi.org/10.1093/jnci/djj102
88. Bosviel R, Dumollard E, Dechelotte P, Bignon YJ, Bernard Gallon D. Can soy phytoestrogens decrease DNA methylation in BRCA1 and BRCA2 oncosuppressor genes in breast cancer?. OMICS. 2012;16(5):235–244. https://doi.org/10.1089/omi.2011.0105
89. King-Batoon A, Leszczynska JM, Klein CB. Modulation of gene methylation by genistein or lycopene in breast cancer cells. Environ Mol Mutagen. 2008;49(1):36–45. https://doi.org/10.1002/em.20363
90. Qin W, Zhu W, Shi H, Hewett JE, Ruhlen RL, MacDonald RS, et al. Soy isoflavones have an antiestrogenic effect and alter mammary promoter hypermethylation in healthy premenopausal women. Nutr Cancer. 2009;61(2):238–244. https://doi.org/10.1080/01635580802404196
91. Li Y, Liu L, Andrews LG, Tollefsbol TO. Genistein depletes telomerase activity through cross-talk between genetic and epigenetic mechanisms. Int J Cancer. 2009;125(2):286– 296. https://doi.org/10.1002/ijc.24398
92. Paluszczak J, Krajka-Kuzniak V, Baer-Dubowska W. The effect of dietary polyphenols on the epigenetic regulation of gene expression in MCF7 breast cancer cells. Toxicol Lett. 2010;192(2):119–125. https://doi.org/10.1016/j.toxlet.2009.10.010
93. Papoutsis AJ, Lamore SD, Wondrak GT, Selmin OI, Romagnolo DF. Resveratrol prevents epigenetic silencing of BRCA-1 by the aromatic hydrocarbon receptor in human breast cancer cells. J Nutr. 2010;140(9):1607–1614. https://doi.org/10.3945/jn.110.123422
94. Harris RM, Waring RH. Diethylstilboestrol - a long term legacy. Maturitas. 2012;72(2):108–112. https://doi.org/10.1016/j.maturitas.2012.03.002
95. Herbst AL, Ulfelder H, Poskanzer DC. Adenocarcinoma of the vagina. Association of maternal stilbestrol therapy with tumor appearance in young women. N Engl J Med. 1971;284(15):878– 881. https://doi.org/10.1056/NEJM197104222841604
96. Sato K, Fukata H, Kogo Y, Ohgane J, Shiota K, Mori C. Neonatal exposure to diethylstilbestrol alters expression of DNA methyl-transferases and methylation of genomic DNA in the mouse uterus. Endocr J. 2009;56(1):131–139. https://doi.org/10.1507/endocrj.K08E-239
97. Doherty LF, Bromer JG, Zhou Y, Aldad TS, Taylor HS. In utero exposure to diethylstilbestrol (DES) or bisphenol-A (BPA) increases EZH2 expression in the mammary gland: an epigenetic mechanism linking endocrine disruptors to breast cancer. Horm Cancer. 2010;1(3):146–155. https://doi.org/10.1007/s12672-010-0015-9
98. Hsu PY, Deatherage DE, Rodriguez BA, Liyanarachchi S, Weng YI, Zuo T, et al. Xenoestrogen-induced epigenetic repression of microRNA-9-3 in breast epithelial cells. Cancer Res. 2009;69(14):5936–5945. https://doi.org/10.1158/0008-5472.CAN-08-4914
99. Weng YI, Hsu PY, Liyanarachchi S, Liu, J, Deatherage DE, Huang YW, et al. Epigenetic influences of low-dose bisphenol A in primary human breast epithelial cells. Toxicol Appl Pharmacol. 2010;248(2):111-121. https://doi.org/10.1016/j.taap.2010.07.014
100. Qin XY, Fukuda T, Yang L, Zaha H, Akanuma H, Zeng Q, et al. Effects of bisphenol A exposure on the proliferation and senescence of normal human mammary epithelial cells. Cancer Biol Ther. 2012;13(5):296-306. https://doi.org/10.4161/cbt.18942

Details

Primary Language

Turkish

Subjects

Pharmaceutical Toxicology

Journal Section

Review

Authors

Ela Tuğrul Karataş ^*
0000-0001-7372-709X
Türkiye

Muhammet Osman Karataş
0009-0002-1883-1438
Türkiye

Sibel Özden
0000-0002-1662-2504
Türkiye

Publication Date

June 1, 2024

Submission Date

January 23, 2024

Acceptance Date

March 25, 2024

Published in Issue

Year 2024 Volume: 44 Number: 2

DOI

https://doi.org/10.52794/hujpharm.1424049

IZ

https://izlik.org/JA42RA37JP

Cite

RIS / Bibtex

APA

Tuğrul Karataş, E., Karataş, M. O., & Özden, S. (2024). Meme Kanseri Epigenetiğinde Biyobelirteçler: Çevresel Faktörlerin Etkisi. Hacettepe University Journal of the Faculty of Pharmacy, 44(2), 165-181. https://doi.org/10.52794/hujpharm.1424049

AMA

1.Tuğrul Karataş E, Karataş MO, Özden S. Meme Kanseri Epigenetiğinde Biyobelirteçler: Çevresel Faktörlerin Etkisi. HUJPHARM. 2024;44(2):165-181. doi:10.52794/hujpharm.1424049

Chicago

Tuğrul Karataş, Ela, Muhammet Osman Karataş, and Sibel Özden. 2024. “Meme Kanseri Epigenetiğinde Biyobelirteçler: Çevresel Faktörlerin Etkisi”. Hacettepe University Journal of the Faculty of Pharmacy 44 (2): 165-81. https://doi.org/10.52794/hujpharm.1424049.

EndNote

Tuğrul Karataş E, Karataş MO, Özden S (June 1, 2024) Meme Kanseri Epigenetiğinde Biyobelirteçler: Çevresel Faktörlerin Etkisi. Hacettepe University Journal of the Faculty of Pharmacy 44 2 165–181.

IEEE

[1]E. Tuğrul Karataş, M. O. Karataş, and S. Özden, “Meme Kanseri Epigenetiğinde Biyobelirteçler: Çevresel Faktörlerin Etkisi”, HUJPHARM, vol. 44, no. 2, pp. 165–181, June 2024, doi: 10.52794/hujpharm.1424049.

ISNAD

Tuğrul Karataş, Ela - Karataş, Muhammet Osman - Özden, Sibel. “Meme Kanseri Epigenetiğinde Biyobelirteçler: Çevresel Faktörlerin Etkisi”. Hacettepe University Journal of the Faculty of Pharmacy 44/2 (June 1, 2024): 165-181. https://doi.org/10.52794/hujpharm.1424049.

JAMA

1.Tuğrul Karataş E, Karataş MO, Özden S. Meme Kanseri Epigenetiğinde Biyobelirteçler: Çevresel Faktörlerin Etkisi. HUJPHARM. 2024;44:165–181.

MLA

Tuğrul Karataş, Ela, et al. “Meme Kanseri Epigenetiğinde Biyobelirteçler: Çevresel Faktörlerin Etkisi”. Hacettepe University Journal of the Faculty of Pharmacy, vol. 44, no. 2, June 2024, pp. 165-81, doi:10.52794/hujpharm.1424049.

Vancouver

1.Ela Tuğrul Karataş, Muhammet Osman Karataş, Sibel Özden. Meme Kanseri Epigenetiğinde Biyobelirteçler: Çevresel Faktörlerin Etkisi. HUJPHARM. 2024 Jun. 1;44(2):165-81. doi:10.52794/hujpharm.1424049

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Mevcut Yapıların Yıkım-Söküm Süreçlerinde Ortaya Çıkan Risklerin Azaltılması: Bir Model Önerisi

Afet ve Risk Dergisi

https://doi.org/10.35341/afet.1529344