Abstract
The contribution of the non-coding genome to disease and its therapeutic potential have been largely unexplored. Recently, several epigenetic drugs developed for cancer treatment have been described to mediate therapeutic effects through the reactivation of the expression of transposable elements in cancer cells. This event activates innate immunity-related pathways and promotes the generation of neoantigens in tumor cells, improving the efficacy of immunotherapeutic treatments. This review focuses on the regulation of transposable elements by epigenetic inhibitors and its implications for immuno-oncology.
Highlights
Studies addressing the etiology and treatment of human diseases have focused on the role of coding genes
Several immuno-oncology approaches are based on the expression of these tumor-specific antigens, which might be present in the cancer cell surface or processed and presented by the major histocompatibility complex (MHC) class I molecules as immunogenic peptides (Figure 1)
L1 elements are 6–7 kb a 50 UTR region with a CpG island that acts as an internal promoter for RNA Polymerase II (Pol II), long, contain a 5′ UTR region with a CpG island that acts as an internal promoter for RNA Polymerase two open reading frames (ORF) that encode for proteins involved in transposition, and a 30 UTR with
Summary
Studies addressing the etiology and treatment of human diseases have focused on the role of coding genes. Current anti-cancer strategies include the use of small molecules that function as inhibitors of enzymes able to modify DNA or histone tails. Some of these enzymes play critical roles in silencing the expression of non-coding elements of the genome. Their inhibition leads to a subsequent derepression of these elements that contributes to increase the immunogenicity of tumors. This review focuses on the role of epigenetics in the silencing of non-coding elements and how epigenetic drugs impact in their expression and provide opportunities to reactivate immune responses against tumors
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