ArticleNucleic acids research2017
Crosstalk between androgen and pro-inflammatory signaling remodels androgen receptor and NF-κB cistrome to reprogram the prostate cancer cell transcriptome.
Article in Nucleic acids research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
55 citing papers in PubMed, 1 synthesis or guideline pooled it, 83 citations in OpenAlex.
- Meta-analysis of Chromatin Programming by Steroid Receptors.Cell reports · 2019Pooled it
- Article
- Sex differences in non-reproductive cancers: mechanistic roles of sex-hormone signaling.Cell communication and signaling : CCS · 2026Review
- A Fully Human Engineered Bone Niche With Endogenous Osteoclastogenesis Reveals Osteoclast-Dependent Osteomimicry in Prostate Cancer Cells.Advanced healthcare materials · 2026Article
- Deciphering the eRNA landscape and revealing target aberrant pathways in prostate cancer.BMC cancer · 2026Article
- Oncolytic virus OH2 induces PD-L1 upregulation via NF-κB signaling and synergizes with anti-PD-L1 therapy in prostate cancer through a targeted extracellular vesicle delivery system.Journal for immunotherapy of cancer · 2026Article
- Combined Dihydroartemisinin and Eupatilin Suppress Prostate Cancer through AR-Associated Ferroptosis and Modulation of Macrophage-Tumor Crosstalk.Research (Washington, D.C.) · 2026Article
- Prostate Cancer: Etiology, Diagnosis, and Treatment.Serican journal of medicine · 2026Article
- Androgen receptor-mediated assisted loading of the glucocorticoid receptor modulates transcriptional responses in prostate cancer cells.Genome research · 2025Article
- TF Profiler: a transcription factor inference method that broadly measures transcription factor activity and identifies mechanistically distinct networks.Genome biology · 2025Article
- Role of SIRT7 in Prostate Cancer Progression: New Insight Into Potential Therapeutic Target.Cancer medicine · 2025Review
- SNP rs9364554 Modulates Androgen Receptor Binding and Drug Response in Prostate Cancer.Biomolecules · 2025Article
- Use of Network Pharmacology and Experiment Validation to Uncover the Mechanism of Jianshen Lishui Prescription in the Treatment of Intracerebral Hemorrhage.Combinatorial chemistry & high throughput screening · 2025Article
- ZBTB18 regulates cytokine expression and affects microglia/macrophage recruitment and commitment in glioblastoma.Communications biology · 2024Article
- Insight into prostate cancer osteolytic metastasis by RelB coordination of IL-8 and S100A4.Clinical and translational medicine · 2024Article
- Dihydrotestosterone Enhances MICA-Mediated Immune Responses to Epstein-Barr Virus-Associated Gastric Carcinoma.Cancers · 2024Article
- Multiplex imaging of localized prostate tumors reveals altered spatial organization of AR-positive cells in the microenvironment.iScience · 2024Article
- SIX2 promotes cell plasticity via Wnt/β-catenin signalling in androgen receptor independent prostate cancer.Nucleic acids research · 2024Article
- Secreted factors from M1 macrophages drive prostate cancer stem cell plasticity by upregulating NANOG,Oncoimmunology · 2024Article
- The Androgen Receptor Does Not Directly Regulate the Transcription of DNA Damage Response Genes.Molecular cancer research : MCR · 2023Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Inflammatory processes and androgen signaling are critical for the growth of prostate cancer (PC), the most common cancer among males in Western countries. To understand the importance of potential interplay between pro-inflammatory and androgen signaling for gene regulation, we have interrogated the crosstalk between androgen receptor (AR) and NF-κB, a key transcriptional mediator of inflammatory responses, by utilizing genome-wide chromatin immunoprecipitation sequencing and global run-on sequencing in PC cells. Co-stimulation of LNCaP cells with androgen and pro-inflammatory cytokine TNFα invoked a transcriptome which was very distinct from that induced by either stimulation alone. The altered transcriptome that included gene programs linked to cell migration and invasiveness was orchestrated by significant remodeling of NF-κB and AR cistrome and enhancer landscape. Although androgen multiplied the NF-κB cistrome and TNFα restrained the AR cistrome, there was no general reciprocal tethering of the AR to the NF-κB on chromatin. Instead, redistribution of FOXA1, PIAS1 and PIAS2 contributed to the exposure of latent NF-κB chromatin-binding sites and masking of AR chromatin-binding sites. Taken together, concomitant androgen and pro-inflammatory signaling significantly remodels especially the NF-κB cistrome, reprogramming the PC cell transcriptome in fashion that may contribute to the progression of PC.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.