**7. Conclusions**

The SWI/SNF complex has been shown to be a central regulator in DNA repair, over other epigenetic complexes such as Polycomb repressive complex 1 (PRC1) and 2 (PRC2), which require the cooperation of their subunits and epigenetic markers to trigger the on–off signaling cascade, generated by acetylation, methylation, or ubiquitination of genes involved in response to DNA damage. We see that participation of epigenetics in the cellular responses goes far beyond DNA promoter methylation and histone modification. Methylation of RNA has a critical role in cell maintenance, changing our notion about RNA functions. We do not know whether deregulation of the m6A machinery could result in cancer development or progression by altering DNA damage response, but knowledge of molecular mechanisms of regulation of m6A cellular modification in tumor cells may develop a combined therapy for m6A regulator proteins as targets that facilitate a better cancer response.

**179**

México

**Author details**

María José López-Ibarra1

Polytechnic Institute, CDMX, México

provided the original work is properly cited.

\*Address all correspondence to: ehdezc@yahoo.com

and Marta Elena Hernández-Caballero2

1 Department of Biochemistry, National School of Biological Sciences, National

2 Faculty of Medicine, Benemérita Autonomous University of Puebla, Puebla,

© 2020 The Author(s). Licensee IntechOpen. This chapter is distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/ by/3.0), which permits unrestricted use, distribution, and reproduction in any medium,

\*

*Epigenetics and DNA Repair in Cancer DOI: http://dx.doi.org/10.5772/intechopen.94030*
