Evidence map›Paper›PMID 27689328›Full record

ArticleOncotarget2016

c-MYC drives histone demethylase PHF8 during neuroendocrine differentiation and in castration-resistant prostate cancer.

Peterson Kariuki Maina, Peng Shao, Qi Liu, Ladan Fazli, Scott Tyler, Moman Nasir, Xuesen Dong, Hank Heng Qi

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed, 1 pooled it
4.1field-weighted citation impact, top 6% of its field
1 · What the graph read from 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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

38 citing papers in PubMed, 1 synthesis or guideline pooled it, 55 citations in OpenAlex.

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  12. Targeting Key Players of Neuroendocrine Differentiation in Prostate Cancer.International journal of molecular sciences · 2023
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors at 2 institutions in 2 countries.

Peterson Kariuki MainaDepartment of Anatomy and Cell Biology, Carver College of Medicine, University of Iowa, Iowa City, IA 52246, USA.
Peng ShaoDepartment of Anatomy and Cell Biology, Carver College of Medicine, University of Iowa, Iowa City, IA 52246, USA.
Qi LiuDepartment of Anatomy and Cell Biology, Carver College of Medicine, University of Iowa, Iowa City, IA 52246, USA.
Ladan FazliVancouver Prostate Center, Department of Urology Sciences, University of British Columbia, Vancouver, BC V6H 3Z6, Canada.
Scott TylerDepartment of Anatomy and Cell Biology, Carver College of Medicine, University of Iowa, Iowa City, IA 52246, USA.
Moman NasirDepartment of Health and Human Physiology, College of Liberal Arts and Sciences, University of Iowa, Iowa City, IA 52242, USA.
Xuesen DongVancouver Prostate Center, Department of Urology Sciences, University of British Columbia, Vancouver, BC V6H 3Z6, Canada.
Hank Heng QiDepartment of Anatomy and Cell Biology, Carver College of Medicine, University of Iowa, Iowa City, IA 52246, USA.
University of Iowa · USUniversity of British Columbia · CA

Funding

Viral VectorP30CA086862 · NCI · UNIVERSITY OF IOWA · PI Christopher K Laubenthal · 2000 to 2026
$70.0M
UNIVERSITY OF IOWA CTSA FOR PEDIATRIC RESEARCHUL1RR024979 · NCRR · UNIVERSITY OF IOWA · PI ROSENTHAL, GARY E · 2007 to 2011
$31.8M
UI INITIATIVE FOR MINORITY STUDENT DEVELOPMENT PROGRAMR25GM058939 · NIGMS · UNIVERSITY OF IOWA · PI ADAMS-PHILLIPS, LORI C, FORBES, TORI · 1999 to 2021
$6.9M
NCI NIH HHS P30 CA086862NCRR NIH HHS UL1 RR024979NIGMS NIH HHS R25 GM058939
6 · The paper itself

Abstract

Epigenetic factors play critical roles in prostate cancer (PCa) development. However, how they contribute to neuroendocrine differentiation (NED) and castration-resistant PCa (CRPC) is not fully understood. Using bioinformatics and biochemical approaches to analyze cell-based models of NED and CRPC, we found a cluster of epigenetic factors whose expression is downregulated during NED and upregulated in CRPC (i.e. follow a Down-Up pattern). Two histone demethylases within this cluster, PHF8 and KDM3A, are post-transcriptionally regulated by c-MYC through miR-22, which targets both PHF8 and KDM3A. We also found that the c-MYC/miR-22/PHF8 axis is downstream of androgen receptor (AR) signaling in CRPC cells. The co-expression of PHF8 with AR in clinical CRPC samples, normal mouse prostate, and adenocarcinomas of the prostate during PCa progression in a transgenic (TRAMP) mouse model supports the connection between PHF8 and AR. Knockdown of PHF8 impedes cell cycle progression in CRPC cells and has more profound effects on their growth than on the parental LNCaP cell line. Furthermore, PHF8 knockdown sensitizes LNCaP-Abl cells to the AR antagonist enzalutamide. Our data reveal novel mechanisms that underlie the regulation of PHF8 and KDM3A during NED and in CRPC, and support the candidacy of PHF8 as a therapeutic target in CRPC.

Indexed as

Genes, myc3' Untranslated RegionsAnimalsCell CycleCell Cycle CheckpointsCell Line, TumorCell ProliferationCell SurvivalEpigenesis, GeneticGene Expression ProfilingGene Expression Regulation, NeoplasticHistone DemethylasesHumansInterleukin-6Jumonji Domain-Containing Histone DemethylasesMale3' Untranslated RegionsHistone DemethylasesInterleukin-6Jumonji Domain-Containing Histone DemethylasesKDM3A protein, humanMicroRNAsMIRN22 microRNA, humanPHF8 protein, humanReceptors, AndrogenTranscription Factorsc-MYCCRPCNEDPHF8prostate cancer

Identifiers

PMID27689328
PMCPMC5342763
OpenAlexW2442109640

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.