[an error occurred while processing this directive]
Review

Epigenetics in the genesis and development of cancers

Expand
  • College of Informatics, National Key Laboratory of Crop Genetic Improvement, Agricultural Bioinformatics Key Laboratory of Hubei Province, Hubei Engineering Technology Research Center of Agricultural Big Data, Huazhong Agricultural University, Wuhan 430070, China

Received date: 2019-05-03

  Revised date: 2019-06-08

  Online published: 2019-06-11

Supported by

Supported by the National Natural Science Foundation of China(31771402);Fundamental Research Funds for the Central Universities(2662017PY116)

Abstract

Cancer is a complex disease caused by the malignant cellular proliferation and metastasis. Elucidating its pathogenic mechanism is one of the major challenges that we face currently. Epigenetic mechanisms are essential for maintaining specific patterns of gene expression and normal development and growth of living individuals. Disorders of epigenetic markers, such as histone modification, DNA/RNA methylation, and changes in the three-dimensional conformation of chromatin, can interfere with gene expression to some extent, and result in cancers. This review provides a brief overview of epigenetics, focusing on their association with the genesis of cancers, and we look forward to the application of epigenetics in cancer clinical diagnosis and treatment.

Cite this article

Jingwen Zhang,Qian Xu,Guoliang Li . Epigenetics in the genesis and development of cancers[J]. Hereditas(Beijing), 2019 , 41(7) : 567 -581 . DOI: 10.16288/j.yczz.19-077

References

[1] Waddington CH . The epigenotype. Int J Epidemiol, 2011,41(1):10-13.
[2] Allis CD, Jenuwein T . The molecular hallmarks of epigenetic control. Nat Rev Genet, 2016,17(8):487-500.
[3] Dor Y, Cedar H . Principles of DNA methylation and their implications for biology and medicine. Lancet, 2018,392(10149):777-786.
[4] Xiao CL, Zhu S, He M, Chen, Zhang Q, Chen Y, Yu G, Liu J, Xie SQ, Luo F, Liang Z, Wang DP, Bo XC, Gu XF, Wang K, Yan GR . N6-methyladenine DNA modification in the human genome. Mo Cell, 2018, 71(2): 306-318. e7.
[5] Zhao BS, Roundtree IA, He C . Post-transcriptional gene regulation by mRNA modifications. Nat Rev Mol Cell Bio, 2016,18(1):31-42.
[6] Li Z, Weng H, Su R, Weng X, Zuo Z, Li C, Huang H, Nachtergaele S, Dong L, Hu C, Qin X, Tang L, Wang Y, Hong GM, Huang H, Wang X, Chen P, Gurbuxani S, Arnovitz S, Li Y, Li S, Strong J, Neilly MB, Larson RA, Jiang X, Zhang P, Jin J, He C, Chen J . FTO plays an oncogenic role in acute myeloid leukemia as a N 6-methyladenosine RNA demethylase . Cancer Cell, 2016,31(1):127-141.
[7] Cui Q, Shi H, Ye P, Li L, Qu Q, Sun G, Sun G, Lu Z, Huang Y, Yang CG, D. Riggs AD, He C, Shi Y . m 6A RNA methylation regulates the self-renewal and tumorigenesis of glioblastoma stem cells . Cell Rep, 2017,18(11):2622-2634.
[8] Zhang S, Zhao BS, Zhou A, Lin K, Zheng S, Lu Z, Chen Y, Sulman EP, Xie K, Bögler O, Majumder S, He C, Huang S . m 6A demethylase ALKBH5 maintains tumorigenicity of glioblastoma stem-like cells by sustaining FOXM1 expression and cell proliferation program. Cancer Cell, 2017, 31(4): 591-606. e6.
[9] Zhang C, Samanta D, Lu H, Bullen JW, Zhang H, Chen I, He X, Semenza GL . Hypoxia induces the breast cancer stem cell phenotype by HIF-dependent and ALKBH5- mediated m 6A-demethylation of NANOG mRNA . Proc Natl Acad Sci USA, 2016,113(14):E2047-E2056.
[10] Huang H, Weng H, Sun W, Qin X, Shi H, Wu H, Zhao BS, Mesquita A, Liu C, Yuan CL, Hu YC, Hüttelmaier S, Skibbe JR, Su R, Deng X, Dong L, Sun M, Li C, Nachtergaele S, Wang Y, Hu C, Ferchen K, Greis KD, Jiang X, Wei M, Qu L, Guan JL, He C, Yang J, Chen J . Recognition of RNA N 6-methyladenosine by IGF2BP proteins enhances mRNA stability and translation . Nat Cell Biol, 2018,20(3):285-295.
[11] Chen M, Wei L, Law CT, Tsang FH, Shen J, Cheng CL, Tsang LH, Ho DW, Chiu DK, Lee JM, Wong CC, Ng IO, Wong CM . RNA N 6-methyladenosine methyltransferase- like 3 promotes liver cancer progression through YTHDF2- dependent posttranscriptional silencing of SOCS2 . Hepatology (Baltimore, Md), 2018,67(6):2254-2270.
[12] Ma JZ, Yang F, Zhou CC, Liu F, Yuan JH, Wang F, Wang TT, Xu QG, Zhou WP, Sun SH . METTL14 suppresses the metastatic potential of hepatocellular carcinoma by modulating N 6-methyladenosine-dependen
Outlines

/