Evidence map›Paper›PMID 26074876›Full record

ReviewFrontiers in endocrinology2015

TR4 Nuclear Receptor Different Roles in Prostate Cancer Progression.

Shin-Jen Lin, Dong-Rong Yang, Gonghui Li, Chawnshang Chang

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in endocrinology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
0.6field-weighted citation impact, top 40% 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

11 citing papers in PubMed, 14 citations in OpenAlex.

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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

4 authors at 2 institutions in 3 countries.

Shin-Jen LinGeorge Whipple Lab for Cancer Research, Departments of Pathology, Urology, Radiation Oncology and the Wilmot Cancer Center, University of Rochester Medical Center , Rochester, NY , USA.
Dong-Rong YangGeorge Whipple Lab for Cancer Research, Departments of Pathology, Urology, Radiation Oncology and the Wilmot Cancer Center, University of Rochester Medical Center , Rochester, NY , USA ; Department of Urology, The Second Affiliated Hospital of Soochow University , Soochow , China.
Gonghui LiGeorge Whipple Lab for Cancer Research, Departments of Pathology, Urology, Radiation Oncology and the Wilmot Cancer Center, University of Rochester Medical Center , Rochester, NY , USA ; Department of Urology, Sir-Run Run Shaw Hospital, Zhejiang University , Hangzhou , China.
Chawnshang ChangGeorge Whipple Lab for Cancer Research, Departments of Pathology, Urology, Radiation Oncology and the Wilmot Cancer Center, University of Rochester Medical Center , Rochester, NY , USA ; Sex Hormone Research Center, China Medical University Hospital , Taichung , Taiwan.
University of Rochester Medical Center · USSoochow University · CN

Funding

Stromal AR Roles in Prostate Hyperplasia and CancerR01CA156700 · NCI · UNIVERSITY OF ROCHESTER · PI CHANG, CHAWNSHANG, YEH, SHUYUAN · 2011 to 2015
$1.6M
Androgen Receptor in B Cell Development and FunctionsR01DK073414 · NIDDK · UNIVERSITY OF ROCHESTER · PI CHANG, CHAWNSHANG · 2007 to 2010
$1.2M
NCI NIH HHS R01 CA156700NIDDK NIH HHS R01 DK073414
6 · The paper itself

Abstract

Nuclear receptors are important to maintain the tissue homeostasis. Each receptor is tightly controlled and under a very complicated balance. In this review, we summarize the current findings regarding the nuclear receptor TR4 and its role in prostate cancer (PCa) progression. In general, TR4 can inhibit the PCa carcinogenesis. However, when PPARγ is knocked out, activation of TR4 can have an opposite effect to promote the PCa carcinogenesis. Clinical data also indicates that higher TR4 expression is found in PCa tissues with high Gleason scores compared to those tissues with low Gleason scores. In vitro and in vivo studies show that TR4 can promote PCa progression. Mechanism dissection indicates that TR4 inhibits PCa carcinogenesis through regulating the tumor suppressor ATM to reduce DNA damages. On the other hand, in the absence of PPARγ, TR4 tends to increase the stem cell population and epithelial-mesenchymal transition (EMT) via regulating CCL2, Oct4, EZH2, and miRNA-373-3p expression that results in increased PCa carcinogenesis. In opposition to PCa initiation, TR4 can increase PCa metastasis via modulating the CCL2 signals. Finally, targeting TR4 enhances the chemotherapy and radiation therapy sensitivity in PCa. Together, these data suggest TR4 is a key player to control PCa progression, and targeting TR4 with small molecules may provide us a new and better therapy to suppress PCa progression.

Indexed as

ATMPPARprostate cancerTR4TZD

Identifiers

PMID26074876
PMCPMC4445305
OpenAlexW1661034799

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.