Epigenetic Influence on Cancer Metastasis and/or Treatment Resistance
A special issue of Cancers (ISSN 2072-6694).
Deadline for manuscript submissions: closed (15 December 2018) | Viewed by 34766
Special Issue Editor
Interests: DNA methylation; cancer invasion and metastasis in breast and pancreatic cancers; carcinoma-associated fibroblasts; epithelial–mesenchymal transition; AKT signaling pathway; tumor microenvironment and immune evasion
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Special Issue Information
Causes of cancer-related mortality are largely known to be involved with reduced apoptosis, resistant to radiation treatments, refractory to target or cytotoxic chemotherapies, gain of cancer stem cells and migratory potential, as well as augmented metastasis to other vital organs. Although the molecular mechanisms underlying the above mentioned aberrations were partly ascribed to acquired genetic alterations, epigenetic abnormalities were also responsible for cancer progression leading to death.
Epigenetics refers to heritable states of gene expression without alterations to the DNA sequence itself. Epigenetic changes encompass altered DNA methylation, dysregulated histone modification, abnormal chromatin remodeling, as well as aberrant expression of micro-RNAs (miRNAs) and long noncoding RNAs (lncRNAs).
This Special Issue focuses on understanding how various epigenetic programs promote cell proliferation, endow cancer cells undergo epithelial-mesenchymal transition with a gain of cancer stem cells and enhance migratory potential leading to augmented tumor metastasis, as well as increase anabolic glucose metabolism. Meanwhile, the diminished cell apoptosis processes result in treatment failure. Because epigenetic alterations are potential reversibility and relatively stable within tumor specimens, clinical applications evolved from epigenetic studies include not only implementing therapies to correct the aberrant epigenomes, but also developing epigenetics-based biomarkers.
Dr. Huey-Jen Lin
Guest Editor
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