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Integrative analysis of ultra-deep RNA-seq reveals alternative promoter usage as a mechanism of activating oncogenic programmes during prostate cancer progression
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Integrative analysis of ultra-deep RNA-seq reveals alternative promoter usage as a mechanism of activating oncogenic programmes during prostate cancer progression
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Journal Article
Integrative analysis of ultra-deep RNA-seq reveals alternative promoter usage as a mechanism of activating oncogenic programmes during prostate cancer progression
2024
Overview
Transcription factor (TF) proteins regulate gene activity by binding to regulatory regions, most importantly at gene promoters. Many genes have alternative promoters (APs) bound by distinct TFs. The role of differential TF activity at APs during tumour development is poorly understood. Here we show, using deep RNA sequencing in 274 biopsies of benign prostate tissue, localized prostate tumours and metastatic castration-resistant prostate cancer, that AP usage increases as tumours progress and APs are responsible for a disproportionate amount of tumour transcriptional activity. Expression of the androgen receptor (AR), the key driver of prostate tumour activity, is correlated with elevated AP usage. We identified
AR
,
FOXA1
and
MYC
as potential drivers of AP activation. DNA methylation is a likely mechanism for AP activation during tumour progression and lineage plasticity. Our data suggest that prostate tumours activate APs to magnify the transcriptional impact of tumour drivers, including
AR
and
MYC
.
With ultra-deep RNA sequencing, Zhang et al. report increased usage of alternative promoters driven by AR, FOXA1 and MYC during prostate cancer progression and suggest altered DNA methylation as a potential underlying mechanism.
Publisher
Nature Publishing Group UK,Nature Publishing Group
Subject
/ Biomedical and Life Sciences
/ Biopsy
/ DNA
/ Gene Expression Regulation, Neoplastic
/ Hepatocyte Nuclear Factor 3-alpha - genetics
/ Hepatocyte Nuclear Factor 3-alpha - metabolism
/ Humans
/ Male
/ Promoter Regions, Genetic - genetics
/ Prostatic Neoplasms - genetics
/ Prostatic Neoplasms - metabolism
/ Prostatic Neoplasms - pathology
/ Prostatic Neoplasms, Castration-Resistant - genetics
/ Prostatic Neoplasms, Castration-Resistant - metabolism
/ Prostatic Neoplasms, Castration-Resistant - pathology
/ Proto-Oncogene Proteins c-myc - genetics
/ Proto-Oncogene Proteins c-myc - metabolism
/ Receptors, Androgen - genetics
/ Receptors, Androgen - metabolism
/ RNA
/ RNA-Seq
/ Tumors
