Unveiling the role of epigenetics in resistance to prostate cancer therapy
Testosterone and other androgen hormones exert their function by binding to the androgen receptor (AR) that acts as a transcription factor and activates the expression of specific target genes. In prostate cancer, inhibition of AR signalling constitutes the backbone of therapy, but resistance eventually develops. The EU-funded RegARcis project is investigating the mechanism underlying this resistance by focussing on chromatin-remodelling complexes. In particular, scientists will study the switch/sucrose non-fermentable (SWI/SNF) factors implicated in nucleosome rearrangement and chromatin accessibility. The idea is to determine potential redistribution of AR binding sites that may explain therapy resistance in advanced stages of the disease.
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