Abstract
Epigenetic alterations are associated with major pathologies including cancer. Epigenetic dysregulation, such as aberrant histone acetylation, altered DNA methylation, or modified chromatin organization, contribute to oncogenesis by inactivating tumor suppressor genes and activating oncogenic pathways. Targeting epigenetic cancer hallmarks can be harnessed as an immunotherapeutic strategy, exemplified by the use of pharmacological inhibitors of DNA methyltransferases (DNMT) and histone deacetylases (HDAC) that can result in the release from the tumor of danger-associated molecular patterns (DAMPs) on one hand and can (re-)activate the expression of tumor-associated antigens on the other hand. This finding suggests that epigenetic modifiers and more specifically the DNA methylation status may change the interaction of chromatin with chaperon proteins including HMGB1, thereby contributing to the antitumor immune response. In this review, we detail how epigenetic modifiers can be used for stimulating therapeutically relevant anticancer immunity when used as stand-alone treatments or in combination with established immunotherapies.
Highlights
Epigenetic modifications involve all molecular mechanisms affecting gene expression in a reversible, transmissible, and adaptive way without altering the DNA sequence
We provide an overview on epigenetic modifiers used as stand-alone agents combination with antitumor therapies, focusing on their capacity to induce anticancer immune or in combination with antitumor therapies, focusing on their capacity to induce anticancer responses
Epigenetic variations are at the origin of changes in gene expression involved in the manifestation of fatal diseases such as cancer
Summary
Epigenetic modifications involve all molecular mechanisms affecting gene expression in a reversible, transmissible, and adaptive way without altering the DNA sequence. Several mechanisms are considered to induce epigenetic changes, such methylation, histone modification,and and non-coding non-coding RNA-associated gene silencing. Modifications functional RNAs. microRNAs and other non-coding RNAs post-transcriptionally regulate to RNA molecules contribute to cellular transformation, even if such changes occur in non-coding mRNA transcripts involved in all major cellular processes. Epigenetic modifications of histone proteins that play a main role in the process transcription of microRNAs targeting tumor suppressor genes or the oncogenes, tumorigenesis have major repercussions on DNA replication, detectionrespectively, and repair ofpromotes. Lys and loss of trimethylation at Lys residues of histone H4 associated with DNA repetitive sequences, or allelic deletion of the H2AX variant, changes the interaction between chaperon proteins and chromatin, impacting on genomic integrity and eventually the occurrence of cancer [15,16,17].
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