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Epigenetic landscape of advanced prostate cancer

ABSTRACT: Epigenetic landscape of advanced prostate cancer

PROVIDER: PRJNA1078399 | ENA |

REPOSITORIES: ENA

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Epigenetic landscape of advanced prostate cancer

Project description:Prostate cancer is characterized as being histologically and molecularly heterogeneous. Additionally, epigenetic changes play an important role in regulating the progression of prostate cancer. However, epigenetic intraindividual heterogeneity is largely unknown in advanced prostate cancer. Hence, the epigenetic profiles of advanced prostate cancer, including autopsy cases, were investigated.

2024-07-20 | GSE256194 | GEO

N-Myc-mediated epigenetic reprogramming drives lineage plasticity in advanced prostate cancer

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Role of MITF in advanced lethal prostate cancer

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Project description:N-Myc-mediated epigenetic reprogramming drives lineage plasticity in advanced prostate cancer [ChIP-seq]

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N-Myc-mediated epigenetic reprogramming drives lineage plasticity in advanced prostate cancer [RNA-seq]

Project description:N-Myc-mediated epigenetic reprogramming drives lineage plasticity in advanced prostate cancer [RNA-seq]

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N-Myc-mediated epigenetic reprogramming drives lineage plasticity in advanced prostate cancer [RNA-seq]

Project description:Despite recent advances in highly effective androgen receptor (AR)-directed therapies for the treatment of prostate cancer, a significant subset of patients with resistant disease develop AR-null, androgen signaling-indifferent neuroendocrine prostate cancer (NEPC). A majority of these NEPC cases that arise following anti-androgen therapy are driven by the aberrant expression of the transcription factor N-Myc. To define the cell lineage states associated with the development of prostate cancer resistance phenotypes, we analyzed whole transcriptome data from a cohort of primary and metastatic tumors compared to benign tissues. NEPC tumors are significantly enriched for stem cell genes associated with embryonic and neural crest lineages, as well as for neural lineage-defining genes. Analysis of the N-Myc transcriptome, cistrome and chromatin-bound interactome using in vivo (GEMM and human xenografts), in vitro (human prostate cancer cell lines) and ex vivo models (NEPC-patient-derived organoids) revealed that the N-Myc cistrome is androgen-dependent and drives a transcriptional program that leads to epithelial plasticity and the acquisition of clinically-relevant neural lineage markers. Moreover, we show that histone marks specifically associated with lineage-defining genes are epigenetically reprogrammed by N-Myc. Finally, we demonstrate how N-Myc-induced gene expression and epigenetic changes can accurately classify patients with advanced prostate cancer which may provide a molecular signature to inform future therapeutic strategies.

2019-08-26 | GSE117305 | GEO

N-Myc-mediated epigenetic reprogramming drives lineage plasticity in advanced prostate cancer [ChIP-seq]

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Role of MITF in advanced lethal prostate cancer

Project description:Great efforts have been made to identify key molecular aberrations that sustain growth and confer resistance to androgen deprivation therapy (ADT) in advanced prostate cancer (PC), and yet PC remains a lethal disease. Recent years have witnessed the discovery of several master regulator transcription factors that enhance lethal PC aggressiveness and provide actionable targets that may improve patient survival. Here we explore the role of the microphthalmia transcription factor (MITF) in lethal prostate cancer. To identify the mechanisms through which MITF mododulates prostate cancer aggressiveness, we knock-down MITF in three prostate cancer cell lines to identify the MITF regulated effector gene network contributing to lethal prostate cancer. Methods: We compared global transcription of three prostate cancer cell lines transduced with a siRNA control and 2 siRNAs targetting MITF by RNAseq. Results: RNA-seq of MITF knockdown prostate cancer cells uncovered a trasncriptional network of MITF regulated genes Conclusions: MITF regulates a discrette gene network that contributes to prostate cancer aggressiveness

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