Aberrant DNA methylation status of endometriosis: Epigenetics as the pathogenesis, biomarker and therapeutic target

Journal of Obstetrics and Gynaecology Research - Tập 37 Số 7 - Trang 683-695 - 2011
Kaei Nasu1, Yukie Kawano1, Yoshiyuki Tsukamoto2, M. Takano1, Noriyuki Takai1, Haili Li1, Yuichi Furukawa1, Wakana Abe1, Masatsugu Moriyama2, Hisashi Narahara1
1Departments of Obstetrics and Gynecology
2Molecular Pathology, Faculty of Medicine, Oita University, Oita, Japan

Tóm tắt

Abstract

Endometriosis, a common, benign, estrogen‐dependent disease affecting 3–10% of women of reproductive age, is characterized by the ectopic growth of endometrial tissue that is found primarily in the peritoneum, ovaries and rectovaginal septum. Recently, endometriosis has been alternatively described as an immune disease, a genetic disease and a disease caused by exposure to environmental factors, in addition to its usual description as a hormonal disease. In addition, accumulating evidence suggests that various epigenetic aberrations play definite roles in the pathogenesis of endometriosis. Epigenetic alterations reported to date in endometriosis include the genomic DNA methylation of progesterone receptor‐B, E‐cadherin, homeobox A10, estrogen receptor‐β, steroidogenic factor‐1 and aromatase. Aberrant expression of DNA methyltransferases, which attach a methyl group to the 5‐carbon position of cytosine bases in the CpG island of the promoter region and silence the corresponding gene expression, has also been demonstrated in endometriosis. This review summarizes the recent studies on the aberrant DNA methylation status and aberrant expression of DNA methyltransferases, which regulate DNA methylation, in endometriosis. We also discuss the recent information on the diagnostic and therapeutic implications of epigenetic alterations occurring in endometriosis.

Từ khóa


Tài liệu tham khảo

10.1016/S0140-6736(04)17403-5

10.1111/j.1749-6632.2002.tb02781.x

10.1055/s-2003-41319

10.1016/j.bpobgyn.2004.02.001

10.1146/annurev.med.55.091902.103805

10.1210/jc.83.12.4474

10.1210/jc.2004-0354

10.1093/humrep/14.5.1328

10.1210/jc.81.3.1118

10.1210/jc.81.1.174

10.1093/molehr/gah133

10.1007/s004390050524

10.1007/s004390051129

10.1016/S0015-0282(00)01663-0

10.1016/S0165-0378(01)00131-0

10.1126/science.1063443

10.1016/j.cell.2007.02.006

10.1093/embo-reports/kve022

10.1038/nrg816

10.1016/S0092-8674(04)00045-5

10.1038/ng1089

10.1111/j.1365-2958.2007.05767.x

10.1038/35049533

10.1503/cmaj.050774

10.1002/jcb.10464

10.1016/S0304-3835(02)00511-6

10.1128/MCB.24.11.4781-4790.2004

10.1074/jbc.M105747200

10.1007/s00412-009-0221-9

10.1038/nature08514

10.4161/cc.3.8.1070

10.1146/annurev.pharmtox.45.120403.095832

10.1038/nature02625

10.1146/annurev.genom.5.061903.180014

10.1016/S1474-4422(09)70262-5

10.4161/epi.1.2.2766

10.1177/1933719107302913

10.1016/j.ajog.2005.01.034

10.1095/biolreprod.107.061804

10.1210/jc.2007-0494

10.1016/j.fertnstert.2007.03.078

10.1038/nature08752

10.1074/jbc.M403427200

10.1016/S0092-8674(00)81656-6

10.1016/S0168-9525(03)00080-5

10.1074/jbc.M513249200

10.1101/gad.1463706

10.1038/nrg1655

10.1016/j.fertnstert.2006.05.077

10.1093/jn/132.8.2401S

10.1093/jn/128.7.1204

Hsieh CJ, 1998, Hypermethylation of the p16INK4a promoter in colectomy specimens of patients with long‐standing and extensive ulcerative colitis, Cancer Res, 58, 3942

10.1158/0008-5472.CAN-03-3690

Arimoto T, 2003, Genome‐wide cDNA microarray analysis of gene‐expression profiles involved in ovarian endometriosis, Int J Oncol, 22, 551

10.1093/molehr/gah097

10.1016/j.fertnstert.2010.06.024

10.1210/endo.140.10.7070

10.1016/S0015-0282(03)00982-8

10.1016/j.mce.2005.11.041

10.1016/S0015-0282(16)60545-9

10.1210/jc.85.8.2897

10.1095/biolreprod.108.070391

10.1210/en.2006-1692

10.1016/S0015-0282(97)00193-3

10.1002/j.1460-2075.1990.tb08280.x

10.1210/er.18.4.502

10.1128/MCB.14.12.8356

10.1016/0960-0760(94)90190-2

10.1126/science.289.5485.1751

10.1016/j.fertnstert.2007.06.008

10.1016/j.fertnstert.2007.10.049

10.1083/jcb.148.3.399

10.1083/jcb.113.1.173

10.1093/humupd/4.5.724

10.1126/science.2884726

10.1172/JCI1597

10.1038/374460a0

10.1093/molehr/5.9.866

10.1093/molehr/gam005

10.1124/pr.57.3.6

10.1093/humupd/dmi034

10.1038/320134a0

10.1016/0014-5793(96)00782-X

10.1093/molehr/5.7.651

10.1093/molehr/5.8.742

10.1210/endo.138.3.4979

10.1210/en.138.9.4022

10.1210/mend-5-10-1552

10.1016/S0021-9258(19)37129-7

10.1210/me.13.2.239

10.1210/me.2006-0302

10.1095/biolreprod57.3.514

10.1677/erc.0.0060293

10.1093/humrep/dem310

10.1016/j.fertnstert.2007.02.057

10.1096/fasebj.11.1.9034163

10.1210/jc.87.8.3745

10.1128/MCB.18.11.6538

10.1038/30764

10.1038/nrd1930

10.1007/s00109-005-0034-0

10.1056/NEJMra072067

10.1016/S1359-6446(03)02697-7

10.1158/0008-5472.CAN-05-3632

Lin X, 2001, Reversal of GSTP1 CpG island hypermethylation and reactivation of pi‐class glutathione S‐transferase (GSTP1) expression in human prostate cancer cells by treatment with procainamide, Cancer Res, 61, 8611

10.1016/j.canlet.2005.03.053

10.1023/A:1022976528441

Korkmaz A, 2007, Epigenetic regulation: A new research area for melatonin?, J Pineal Res, 44, 41, 10.1111/j.1600-079X.2007.00509.x

10.1074/jbc.M209839200

Ushijima T, 2005, Detection and interpretation of altered methylation patterns in cancer cells, Nature, 5, 223

10.1007/BF03194647

10.1016/S0301-2115(99)00263-8

Fiegl H, 2004, Methylated DNA collected by tampons–a new tool to detect endometrial cancer, Cancer Epidemiol Biomarkers Prev, 13, 882, 10.1158/1055-9965.882.13.5

10.1093/molehr/gap064