ArticleMolecular biology reports2014
ChIP-seq analysis of androgen receptor in LNCaP cell line.
Article in Molecular biology reports, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 3 papers.
What it found
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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
3 citing papers in PubMed, 9 citations in OpenAlex.
- Castration Resistance in Prostate Cancer Is Mediated by the Kinase NEK6.Cancer research · 2017Article
- Regulation of c-Myc expression by the histone demethylase JMJD1A is essential for prostate cancer cell growth and survival.Oncogene · 2016Article
- Article
Corrections and comments
- Retraction · 2015-08-18Compromised Peer Review · Investigation by Journal/Publisher · · 2/21/2017
- Retracted
Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The aim of this study was to screen target genes and gene functions of androgen receptor (AR) in LNCaP cell line by ChIP-seq data analysis. We downloaded the gene expression profile GSE14092 from Gene Expression Omnibus database and selected ChIP-seq data (GSM353644) of AR stimulated by androgen R1881 (R1881 stimulation group) and the ChIP-seq data (GSM353643) of AR without R1881 stimulation (control group). MACS peak calling software was used to identify the AR binding cites. After target genes selection and function analysis, motif finding analysis was utilized to predict the AR co-located transcription regulation factors, and we analyzed their functions through GO enrichment analysis. Total 27202 and 2730 AR binding sites were detected in the R1881 stimulation group and the control group, respectively and 398 and 58 target genes were identified in R1881 stimulation group and control group, respectively. Based on GO enrichment analysis, 20 biological processes which AR regulated in the LNCaP cells were enriched, including xenobiotic metabolic process, positive regulation of interleukin-2 production and cellular response to sterol etc. We finally identified 99 transcription factors with high motif enrichment significant levels, and the enrichment of AR co-located transcription factors was significantly enriched in the biological process of regulation of cell proliferation in which 13 transcription factors were involved (FOXJ1, FOXM1, NF1, SOX2, HOXD13, FOXO1, FOXP3, FOXO4, SOX9, PGR, DBP, JUN and TLX1). The analysis of AR target genes and gene functions help us to elucidate the mechanism of the prostate cancer on a molecular level. In addition, it will pave the way to effective therapies for prostatic cancer. However, further experiments are still needed to confirm our results.
Identifiers
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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.