Epigenetic factors in breast cancer therapy

Abstract

Epigenetic modifications are inherited differences in cellular phenotypes, such as cell gene expression alterations, that occur during somatic cell divisions (also, in rare circumstances, in germ line transmission), but no alterations to the DNA sequence are involved. Histone alterations, polycomb/trithorax associated proteins, short non-coding or short RNAs, long non-coding RNAs (lncRNAs), & DNA methylation are just a few biological processes involved in epigenetic events. These various modifications are intricately linked. The transcriptional potential of genes is closely conditioned by epigenetic control, which is crucial in normal growth and development. Epigenetic mechanisms transmit genomic adaptation to an environment, resulting in a specific phenotype. The purpose of this systematic review is to glance at the roles of Estrogen signalling, polycomb/trithorax associated proteins, DNA methylation in breast cancer progression, as well as epigenetic mechanisms in breast cancer therapy, with an emphasis on functionality, regulatory factors, therapeutic value, and future challenges.

Keywords: breast; cancer; epigenetics; estrogen; therapy.

FIGURE 1

Epigenetic Deregulation in Cancer. A vast number of epigenetic modifiers are mutated or activated inappropriately during cancer genesis. Simultaneously, epigenetic alterations such as DNA methylation, histone modifications, and microRNAs cause aberrant gene expression, resulting in genomic instability.

FIGURE 2

Wnt Signalling Pathway: DKK3 binds to LRP, a WNT pathway coactivator of Frizzled, in normal mammary epithelial cells, preventing the pathway from being activated in the presence of the WNT ligand. In the absence of WNT activation, E-Cadherin binds to cytoplasmic -catenin, which is destroyed by GSK3. The DKK3 promoter, on the other hand, is hypermethylated in breast cancer, resulting in its downregulation. LRP can coactivate Frizzled in the presence of the WNT ligand in the absence of DKK3, resulting in phosphorylation of DSH, which prevents GSK3 from degrading -catenin.