Abstract
Acquired drug resistance is a major problem in the treatment of many diseases, including cancer. It has been associated with selection of cells displaying hypomethylation of enhancer of cell proliferation (PTPN6) and drug efflux gene promoters (ABCB1), as well as hypermethylation of promoter regions of pro-apoptotic genes (APAF1, DAPK1, DOK2), or altered promoter methylation patterns of DNA repair genes (AGF, FANCF, MLH1, SRBC). Promoter hypomethylation of PTPN6 can favor the efflux of drugs, proliferation, and differentiation, and thereby the selection of tumor cell subpopulations that are resistant to chemotherapy. In addition, hypomethylation of many other genes can favor accumulation of somatic mutation and apoptosis resistance and thus the selection of resistant tumor cell subpopulations. The important contribution of DNA methylation in drug resistance implies the possibility of preventing or abolishing drug resistance by reverting the cancer epigenome of non-responsive cells to a drug-responsive state.
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