3D Genome Architecture and Epigenetic Regulation of Lineage Identity in Advanced Prostate Cancer

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ID: 317628
2026
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Abstract
Prostate cancer development and progression depend on androgen receptor (AR) signaling. Therefore, androgen-deprivation therapy (ADT) and AR signaling inhibitors (ARSIs) are standard therapies for advanced or metastatic disease. Although these treatments are initially effective, prostate cancer inevitably progresses to a lethal stage termed castration-resistant prostate cancer (CRPC). In the majority of patients, CRPC occurs via re-activation of AR signaling (CRPC-AR). However, lineage plasticity is a hallmark of cancer that drives AR-independent CRPC phenotypes in a subset of patients. One subtype of AR-negative CRPC is neuroendocrine prostate cancer (NEPC), which transforms from CRPC-AR by losing the characteristic AR-driven luminal epithelial identity and gaining neuroendocrine identity. Another AR-negative CRPC subtype lacks AR and neuroendocrine features and has therefore been classified as double-negative prostate cancer (DNPC). Chromatin modifications, alterations in three-dimensional (3D) genome structure, and expression of transcriptional regulators are crucial for controlling lineage states and modulating AR-dependent and AR-independent phenotypes in CRPC. Here, we highlight how high-resolution investigations of the 3D genome have revealed interdependence between chromatin architecture and transcriptional regulation, offering novel insights into the mechanisms of CRPC progression and context-specific targets for therapeutic intervention.
Reference Key
openalex_W7165019270 Use this key to autocite in the manuscript while using SciMatic Manuscript Manager or Thesis Manager
Authors Songyan Qi, Scott M. Dehm
Journal american journal of physiology endocrinology and metabolism
Year 2026
DOI
10.1210/endocr/bqag068
URL
https://doi.org/10.1210/endocr/bqag068
Keywords Keywords not found

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