• editor.aipublications@gmail.com
  • Track Your Paper
  • Contact Us
  • ISSN: 2456-8015

International Journal Of Medical, Pharmacy And Drug Research(IJMPD)

Role of Epigenetic Factors in Cancer Formation: A Review

Shajeda Akter Nishat , Mohammad Morshad Alam , Abrar Wahab

International Journal of Medical, Pharmacy and Drug Research(IJMPD), Vol-1,Issue-3, September - October 2017, Pages 1-5 ,

Download | Downloads : 6 | Total View : 1236


Epigeneticsrefers to the mechanisms that alter gene expression without altering the primary DNA sequence. Epigenetic modifications are commonly described as important players in cancer progression. They comprise DNA methylation, histone modifications, nucleosome positioning, and small, noncoding microRNAs. The information carried by epigenetic modifications plays a critical part in the regulation of all DNA-based events, such as transcription, DNA repair, and replication. Abnormal expression patterns or genomic modifications in chromatin regulators can have intense results and can lead to the induction and maintenance of various cancers. Epigenetics also represents an attractive opportunity of reverting cancer-specific alterations, which may leadto a possibility of stopping this disease. Epigenetic changes have been identified as putative cancer biomarkers for early detection, disease monitoring, prognosis, and risk assessment. Emerging findings in this area are contributing to cancer management and monitoring, and further progress is expected.

Cancer; epigenetics; DNA methylation; histones modifications; microRNA; epigenetic therapy.

[1] Balgobind, B. V., Zwaan, C. M., Pieters, R., & Van den Heuvel-Eibrink, M. M. (2011). The heterogeneity of pediatric MLL-rearranged acute myeloid leukemia. Leukemia, 25(8), 1239-1248.
[2] Berger, S. L., Kouzarides, T., Shiekhattar, R., &Shilatifard, A. (2009). An operational definition of epigenetics. Genes & development, 23(7), 781-783.
[3] Bhaskara, S., Knutson, S. K., Jiang, G., Chandrasekharan, M. B., Wilson, A. J., Zheng, S., ... & Wells, C. E. (2010). Hdac3 is essential for the maintenance of chromatin structure and genome stability. Cancer cell, 18(5), 436-447.
[4] Bots, M., &Johnstone, R. W. (2009). Rational combinations using HDAC inhibitors. Clinical cancer research, 15(12), 3970-3977.
[5] Cang, S., Ma, Y., & Liu, D. (2009). New clinical developments in histone deacetylase inhibitors for epigenetic therapy of cancer. Journal of hematology & oncology, 2(1), 22.
[6] Chase, A., & Cross, N. C. (2011). Aberrations of EZH2 in cancer. Clinical Cancer Research, 17(9), 2613-2618.
[7] Conerly, M., & Grady, W. M. (2010). Insights into the role of DNA methylation in disease through the use of mouse models. Disease models & mechanisms, 3(5-6), 290-297.
[8] Dawson, M. A., &Kouzarides, T. (2012). Cancer epigenetics: from mechanism to therapy. Cell, 150(1), 12-27.
[9] EinavNili, G. Y., Saito, Y., Egger, G., & Jones, P. A. (2008). Cancer epigenetics: modifications, screening, and therapy. Annu. Rev. Med., 59, 267-280.
[10] Esteller, M. (2007). Cancer epigenomics: DNA methylomes and histone-modification maps. Nature Reviews Genetics, 8(4), 286-298.
[11] Esteller, M. (2008). Epigenetics in cancer. New England Journal of Medicine, 358(11), 1148-59.
[12] Feinberg, A. P., Ohlsson, R., &Henikoff, S. (2006). The epigenetic progenitor origin of human cancer. Nature reviews genetics, 7(1), 21-33.
[13] Greer, E. L., & Shi, Y. (2012). Histone methylation: a dynamic mark in health, disease and inheritance. Nature Reviews Genetics, 13(5), 343-357.
[14] Gui, Y., Guo, G., Huang, Y., Hu, X., Tang, A., Gao, S., ... & He, M. (2011). Frequent mutations of chromatin remodeling genes in transitional cell carcinoma of the bladder. Nature genetics, 43(9), 875-878.
[15] Hargreaves, D. C., & Crabtree, G. R. (2011). ATP-dependent chromatin remodeling: genetics, genomics and mechanisms. Cell research, 21(3), 396-420.
[16] Hayashita, Y., Osada, H., Tatematsu, Y., Yamada, H., Yanagisawa, K., Tomida, S., ... & Takahashi, T. (2005). A polycistronic microRNA cluster, miR-17-92, is overexpressed in human lung cancers and enhances cell proliferation. Cancer research, 65(21), 9628-9632.
[17] Hoque, M. O., Kim, M. S., Ostrow, K. L., Liu, J., Wisman, G. B. A., Park, H. L., ... &Schuuring, E. (2008). Genome-wide promoter analysis uncovers portions of the cancer methylome. Cancer research, 68(8), 2661-2670.
[18] Jones, P. A., &Baylin, S. B. (2007). The epigenomics of cancer. Cell, 128(4), 683-692.
[19] Jones, P. A., & Taylor, S. M. (1980). Cellular differentiation, cytidine analogs and DNA methylation. Cell, 20(1), 85-93.
[20] Kacem, S., &Feil, R. (2009). Chromatin mechanisms in genomic imprinting. Mammalian Genome, 20(9-10), 544-556.
[21] le Sage, C., Nagel, R., Egan, D. A., Schrier, M., Mesman, E., Mangiola, A., ... &Farace, M. G. (2007). Regulation of the p27Kip1 tumor suppressor by miR‐221 and miR‐222 promotes cancer cell proliferation. The EMBO journal, 26(15), 3699-3708.
[22] Lin, H., Wong, R. P., Martinka, M., & Li, G. (2009). Loss of SNF5 expression correlates with poor patient survival in melanoma. Clinical Cancer Research, 15(20), 6404-6411.
[23] Marks, P. A., Rifkind, R. A., Richon, V. M., Breslow, R., Miller, T., & Kelly, W. K. (2001). Histone deacetylases and cancer: causes and therapies. Nature Reviews Cancer, 1(3), 194-202.
[24] McCabe, M. T., Brandes, J. C., &Vertino, P. M. (2009). Cancer DNA methylation: molecular mechanisms and clinical implications. Clinical Cancer Research, 15(12), 3927-3937.
[25] Minucci, S., &Pelicci, P. G. (2006). Histone deacetylase inhibitors and the promise of epigenetic (and more) treatments for cancer. Nature Reviews Cancer, 6(1), 38-51.
[26] Miremadi, A., Oestergaard, M. Z., Pharoah, P. D., & Caldas, C. (2007). Cancer genetics of epigenetic genes. Human molecular genetics, 16(R1), R28-R49.
[27] Peter, M. E. (2009). Let-7 and miR-200 microRNAs: guardians against pluripotency and cancer progression. Cell cycle, 8(6), 843-852.
[28] Rotili, D., & Mai, A. (2011). Targeting histone demethylases: a new avenue for the fight against cancer. Genes & cancer, 2(6), 663-679.
[29] Sadeh, R., & Allis, C. D. (2011). Genome-wide “re”-modeling of nucleosome positions. Cell, 147(2), 263-266.
[30] Shankar, S., &Srivastava, R. K. (2008). Histone deacetylase inhibitors: mechanisms and clinical significance in cancer: HDAC inhibitor-induced apoptosis. In Programmed Cell Death in Cancer Progression and Therapy (pp. 261-298). Springer Netherlands.
[31] Smith, K. T., & Workman, J. L. (2009). Histone deacetylase inhibitors: anticancer compounds. The international journal of biochemistry & cell biology, 41(1), 21-25.
[32] Strahl, B. D., & Allis, C. D. (2000). The language of covalent histone modifications. Nature, 403(6765), 41-45.
[33] Straussman, R., Nejman, D., Roberts, D., Steinfeld, I., Blum, B., Benvenisty, N., ... & Cedar, H. (2009). Developmental programming of CpG island methylation profiles in the human genome. Nature structural & molecular biology, 16(5), 564-571.
[34] Visone, R., Russo, L., Pallante, P., De Martino, I., Ferraro, A., Leone, V., ... & Fusco, A. (2007). MicroRNAs (miR)-221 and miR-222, both overexpressed in human thyroid papillary carcinomas, regulate p27Kip1 protein levels and cell cycle. Endocrine-related cancer, 14(3), 791-798.
[35] Wolff, E. M., Byun, H. M., Han, H. F., Sharma, S., Nichols, P. W., Siegmund, K. D., ... & Liang, G. (2010). Hypomethylation of a LINE-1 promoter activates an alternate transcript of the MET oncogene in bladders with cancer. PLoS Genet, 6(4), e1000917.
[36] Yang, X. J. (2004). The diverse superfamily of lysine acetyltransferases and their roles in leukemia and other diseases. Nucleic acids research, 32(3), 959-976.
[37] Yoo, C. B., & Jones, P. A. (2006). Epigenetic therapy of cancer: past, present and future. Nature reviews Drug discovery, 5(1), 37-50.