Chemoprevention as a way to control epigenetic changes (Analytical review of the literature)
- Authors: Kiselev V.I.1, Ashrafyan L.A.2, Bezhenar V.F.3, Tsypurdeyeva A.A.3
-
Affiliations:
- National Research Centre (NRC) “Kurchatov Institute”
- Russian Scientific Center of Roentgenoradiology (RSCRR)
- D. O. Ott Research Institute of Obstetrics and Gynecology
- Issue: Vol 63, No 4 (2014)
- Pages: 74-79
- Section: Articles
- Submitted: 15.09.2014
- Published: 15.09.2014
- URL: https://journals.eco-vector.com/jowd/article/view/2686
- DOI: https://doi.org/10.17816/JOWD63474-79
- ID: 2686
Cite item
Abstract
Epigenetic alterations have been identified as promising new targets for cancer prevention strategies as they occur early during carcinogenesis. Therapy is mainly focused on reversion of DNA methylation by inhibiting DNA-methyltransferases and low level of acetylated histones by inhibiting histone deacetylases. DIM and epigallocatechin-3-gallate (EGCG) substances are believed to be an anticancer agent in part through its regulation of epigenetic processes. These agents demonstrate efficacy in cancer chemopreventive action and have potential to be used to current cancer therapies.
Full Text
About the authors
Vsevolod Ivanovich Kiselev
National Research Centre (NRC) “Kurchatov Institute”
Email: vkis10@mail.ru
Lev Andreyevich Ashrafyan
Russian Scientific Center of Roentgenoradiology (RSCRR)
Email: levaa2004@yahoo.com
Vitaliy Fedorovich Bezhenar
D. O. Ott Research Institute of Obstetrics and Gynecology
Email: bez-vitaly@yandex.ru
Anna Alekseyevna Tsypurdeyeva
D. O. Ott Research Institute of Obstetrics and Gynecology
Email: iagmail@ott.ru
References
- Azad N. et al. The future of epigenetic therapy in solid tumours - lessons from the past. Nat. Rev. Clin. Oncol. 2013; 10 (5): 256-266.
- Balasubramanian S., Verner E., Buggy J. J. Isoform-specific histone deacetylase inhibitors: the next step? Cancer Lett. 2009; 280 (2): 211-221.
- Banerjee S. et al. Attenuation of multi-targeted proliferation-linked signaling by 3,3'-diindolylmethane (DIM): From bench to clinic. Mutat. Res. 2011;728 (1-2): 47-66.
- Beaulieu N. et al. An essential role for DNA methyltransferase DNMT3B in cancer cell survival. J. Biol. Chem. 2002; 277 (310): 28 176-28 181.
- Beaver L. M. et al. 3,3’-Diindolylmethane, but not indole-3-carbinol, inhibits histone deacetylase activity in prostate cancer cells. Toxicol. Appl. Pharmacol. 2012; 263 (3): 345-351.
- Berdasco M., Esteller M. Aberrant epigenetic landscape in cancer: how cellular identity goes awry. Dev. Cell. 2010; 19 (5): 698-711.
- Berletch J. B. et al. Epigenetic and genetic mechanisms contribute to telomerase inhibition by EGCG. J. Cell Biochem. 2008; 103 (2): 509-519.
- Bhatnagar N. et al. 3,3’-Diindolylmethane enhances the efficacy of butyrate in colon cancer prevention through down-regulation of surviving. Cancer Prev. Res. 2009; 2 (6): 581-589.
- Chen S., Sang N. Histone Deacetylase Inhibitors: The Epigenetic Therapeutics That Repress Hypoxia-Inducible Factors. J. Biomed. Biotechnol. 2011; 2011:197946. doi: 10.1155/2011/197946. Epub 2010 Dec 5.
- Choudhuri S. From Waddington’s epigenetic landscape to small noncoding RNA: some important milestones in the history of epigenetics research. Toxicol. Mech. Methods. 2011; 21 (4): 252-274.
- Deb G. et al. Epigenetic induction of tissue inhibitor of matrix metalloproteinase-3 by green tea polyphenols in breast cancer cells. Mol. Carcinog. 2014; doi: 10.1002/mc.22121.
- Esteller M. CpG island hypermethylation and tumor suppressor genes: a booming present, a brighter future. Oncogene. 2002; 21 (35): 5427-40.
- Esteller M. Epigenetics in cancer. N. Engl. J. Med. 2008; 358 (11): 1148-59.
- Fang M., Chen D., Yang C. S. Dietary polyphenols may affect DNA methylation. J. Nutr. 2007; 137 (1): 223S-8S.
- Fang M. Z. et al. Reversal of hypermethylation and reactivation of p16INK4a, RARbeta, and MGMT genes by genistein and other isoflavones from soy. Clin. Cancer Res. 2005; 11 (19 Pt 1): P. 7033-7041.
- Fang M. Z. et al. Tea polyphenol (-) epigallocatechin-3-gallate inhibits DNA methyltransferase and reactivates methylationsilenced genes in cancer cell lines. Cancer Res. 2003; 63 (22): 7563-7570.
- Gao Z. et al. Promoter demethylation of WIF-1 by epigallocatechin-3-gallate in lung cancer cells. Anticancer Res. 2009; 29 (6): 2025- 30
- Gerhauser C. Cancer chemoprevention and nutriepigenetics: state of the art and future challenges. Top. Curr. Chem. 2013; 329: 73-132.
- Herman J.G, Baylin S. B. Gene silencing in cancer in association with promoter hypermethylation. N. Engl. J. Med. 2003; 349 (21): 2042-2054.
- Herman J. G. Hypermethylation of tumor suppressor genes in cancer. Semin. Cancer Biol. 1999; 9 (5): 359-367.
- Jaenisch R., Bird A. Epigenetic regulation of gene expression: how the genome integrates intrinsic and environmental signals. Nat. Genet. 2003; 33: 245- 54.
- Johnstone R. W., Licht J. D. Histone deacetylase inhibitors in cancer therapy: is transcription the primary target? Cancer Cell. 2003; 4 (1): 13-8.
- Kelly T. K., De Carvalho D. D., Jones P. A. Epigenetic Modifications as Therapeutic Targets. Nat. Biotechnol. 2010; 28 (10): 1069- 1078.
- Lee W.J, Shim J.Y, Zhu B. T. Mechanisms for the inhibition of DNA methyltransferases by tea catechins and bioflavonoids. Mol. Pharmacol. 2005; 68 (4): 1018-1030.
- Li Y., Li X., Guo B. Chemopreventive agent 3,3’-diindolylmethane selectively induces proteasomal degradation of class I histone deacetylases. Cancer Res. 2010; 70 (2): 646-654.
- Lyn-Cook B. D. et al. Gender differences in gemcitabine (Gemzar) efficacy in cancer cells: effect of indole-3-carbinol. Anticancer Res. 2010; 30 (12): 4907-4913.
- Martinez P., Blasco M. A. Telomeric and extra-telomeric roles for telomerase and the telomere-binding proteins. Nat. Rev. Cancer. 2011; 11 (3): 161- 176.
- Meeran S. M. et al. A novel prodrug of epigallocatechin-3-gallate: differential epigenetic hTERT repression in human breast cancer cells. Cancer Prev. Res. 2011; 4 (8): 1243-1254.
- Nandakumar V., Vaid M,. Katiyar S. K. (-)-Epigallocatechin-3-gallate reactivates silenced tumor suppressor genes, Cip1/p21 and p16INK4a, by reducing DNA methylation and increasing histones acetylation in human skin cancer cells. Carcinogenesis. 2011; 32 (4): 537- 544.
- Pandey M., Shukla S., Gupta S. Promoter demethylation and chromatin remodeling by green tea polyphenols leads to re-expression of GSTP1 in human prostate cancer cells. Int. J. Cancer. 2010; 26 (11): 2520-2533.