Evidence map›Paper›PMID 32361123›Full record

ArticleTranslational oncology2020

Adrenergic Blockade Promotes Maintenance of Dormancy in Prostate Cancer Through Upregulation of GAS6.

Ann M Decker, Joseph T Decker, Younghun Jung, Frank C Cackowski, Stephanie Daignault-Newton, Todd M Morgan, Lonnie D Shea, Russell S Taichman

Open access · goldAbstract read
In one paragraph

Article in Translational oncology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
2.0field-weighted citation impact, top 14% 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

12 citing papers in PubMed, 22 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

8 authors at 2 institutions in 1 country.

Ann M DeckerDepartment of Periodontics and Oral Medicine, University of Michigan, Ann Arbor, MI.
Joseph T DeckerDepartment of Biomedical Engineering, University of Michigan, Ann Arbor, MI.
Younghun JungDepartment of Periodontics and Oral Medicine, University of Michigan, Ann Arbor, MI.
Frank C CackowskiDepartment of Periodontics and Oral Medicine, University of Michigan, Ann Arbor, MI; Department of Internal Medicine, Division of Hematology/Oncology, University of Michigan, Ann Arbor, MI.
Stephanie Daignault-NewtonRogel Cancer Center, University of Michigan, Ann Arbor, MI.
Todd M MorganRogel Cancer Center, University of Michigan, Ann Arbor, MI; Department of Urology, University of Michigan, Ann Arbor, MI.
Lonnie D SheaDepartment of Biomedical Engineering, University of Michigan, Ann Arbor, MI.
Russell S TaichmanDepartment of Periodontics and Oral Medicine, University of Michigan, Ann Arbor, MI; School of Dentistry, University of Alabama-Birmingham, Birmingham, AL. Electronic address: taichman@uab.edu.
University of Michigan–Ann Arbor · USUniversity of Alabama at Birmingham · US

Funding

Postdoc Stipend Supplement: Developmental Origins of Metabolic Disorders T32T32DK071212 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI DAVID P OLSON, Kanakadurga Singer · 2005 to 2026
$5.4M
Chimeric Antigen Receptor T Cell Design Through Living Cell Systems BiologyK01EB028877 · NIBIB · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI DECKER, JOSEPH THOMAS · 2019 to 2022
$492k
NIBIB NIH HHS K01 EB028877
6 · The paper itself

Abstract

Men diagnosed with localized prostate cancer can develop metastases many years after initial treatment, resulting in a poor prognosis. The purpose of this study was to investigate the mechanisms by which signaling through norepinephrine (NE) may incite relapse of quiescent prostate cancer. We used an unbiased bioinformatics pipeline to examine mechanisms for recurrence related to sympathetic signaling in the bone marrow. A transcription factor cell array identified ATF1, RAR, and E2F as key nodes in prostate cancer cells exiting quiescence through adrenergic signaling. Subsequent secretome analysis identified GAS6 as affecting activity of these three factors, leading to cell cycle reentry. GAS6 expression was downregulated in osteoblasts through activation of the cAMP pathway and was targeted in vitro and in vivo using pharmacological agents (propranolol and phentolamine). Propranolol increased expression of GAS6 by osteoblasts, and phentolamine significantly inhibited expression. Propranolol treatment was sufficient to both increase GAS6 expression in marrow osteoblasts as well as eliminate the effects of NE signaling on GAS6 expression. These results demonstrate a strong correlation between adrenergic signaling, GAS6 expression, and recurrence in prostate cancer, suggesting a novel therapeutic direction for patients at high risk of metastasis.

Identifiers

PMID32361123
PMCPMC7191848
OpenAlexW3022830515

What OpenQuestion holds

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LicenceCC BY-NC-ND
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.