Background:
Epigenetic alterations comprise key regulatory events that dynamically alter
gene expression and their deregulation is commonly linked to the pathogenesis of various diseases,
including cancer. Unlike DNA mutations, epigenetic alterations involve modifications to proteins and
nucleic acids that regulate chromatin structure without affecting the underlying DNA sequence, altering
the accessibility of the transcriptional machinery to the DNA, thus modulating gene expression. In cancer
cells, this often involves the silencing of tumor suppressor genes or the increased expression of
genes involved in oncogenesis. Advances in laboratory medicine have made it possible to map critical
epigenetic events, including histone modifications and DNA methylation, on a genome-wide scale. Like
the identification of genetic mutations, mapping of changes to the epigenetic landscape has increased
our understanding of cancer progression. However, in contrast to irreversible genetic mutations, epigenetic
modifications are flexible and dynamic, thereby making them promising therapeutic targets. Ongoing
studies are evaluating the use of epigenetic drugs in chemotherapy sensitization and immune
system modulation. With the preclinical success of drugs that modify epigenetics, along with the FDA
approval of epigenetic drugs including the DNA methyltransferase 1 (DNMT1) inhibitor 5-azacitidine
and the histone deacetylase (HDAC) inhibitor vorinostat, there has been a rise in the number of drugs
that target epigenetic modulators over recent years.
Conclusion:
We provide an overview of epigenetic modulations, particularly those involved in cancer,
and discuss the recent advances in drug development that target these chromatin-modifying events,
primarily focusing on novel strategies to regulate the epigenome.
LAT1 and ASCT2 Related microRNAs as Potential New Therapeutic Agents against Colorectal Cancer Progression
