Abstract
An increasingly number of women of all age groups are affected by cancer, despite substantial progress in our understanding of cancer pathobiology, the underlying genomic alterations and signaling cascades, and cellular-environmental interactions. Though our understanding of women’s cancer is far more complete than ever before, there is no comprehensive model to explain the reasons behind the increased incidents of certain reproductive cancer among older as well as younger women. It is generally suspected that environmental and life-style factors affecting hormonal and growth control pathways might help account for the rise of women’s cancers in younger age, as well, via epigenetic mechanisms. Epigenetic regulators play an important role in orchestrating an orderly coordination of cellular signals in gene activity in response to upstream signaling and/or epigenetic modifiers present in a dynamic extracellular milieu. Here we will discuss the broad principles of epigenetic regulation of DNA methylation and demethylation, histone acetylation and deacetylation, and RNA methylation in women’s cancers in the context of gene expression, hormonal action, and the EGFR family of cell surface receptor tyrosine kinases. We anticipate that a better understanding of the epigenetics of women’s cancers may provide new regulatory leads and further fuel the development of new epigenetic biomarkers and therapeutic approaches.
Highlights
Cancer continues to be the second leading cause of mortality globally
Recent studies suggest that EMT associated upregulation of PD-L1 in cancer cells might be regulated in a context-dependent manner—as there was an increased recruitment of an active transcription histone mark (H3K4me3), at the expense of repressive histone marks (H3K9me3, H3K27me3), on the PD-L1 promoter in tumorspheres but not monolayer breast cancer cells [96]
This might be important for two reasons: chromatin remodeling pathways play a mandatory role in executing transcriptional effects of ER and PR, and the fact that environmental and certain phytoestrogens factors are thought to act as modifier of stimulatory effects of hormonal signaling in the endometrial cancer
Summary
Cancer continues to be the second leading cause of mortality globally. The potential causes for the growing cancer incidence are multifactorial: the ever-increasing size of the aging population, gene-environment interactions, and a whole range of intrinsic and extrinsic established and suspected cancer risk factors. Even with dedicated global resources for cancer research and treatment, the underlying molecular basis of most, if not all, human cancers remains largely unknown [5]. The burden of women’s cancers continues to grow despite substantial progress in our understanding of cancer’s pathobiology, underlying genomic alterations and signaling cascades, and cellular-environmental interactions. One key area of promising treatment is epigenetic therapy which is designed to modify the epigenetic status of the target or targets of interest [7]—the benefits of which are yet to be fully translated and realized into meaningful treatments for cancer common in females. We discuss the impact of selective modules of epigenetics, such as DNA and RNA methylation, histone methylation, and histone acetylation, in modifying gene expression in response to upstream signals
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