Evidence map›Paper›PMID 27604827›Full record

ArticleThe Prostate2017

TGF-β Effects on Prostate Cancer Cell Migration and Invasion Require FosB.

Cachétne S X Barrett, Ana C Millena, Shafiq A Khan

Abstract read
In one paragraph

Article in The Prostate, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.

0numbers the graph read from it
0cells of the map it votes in
53citing papers in PubMed
3.8field-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

53 citing papers in PubMed, 96 citations in OpenAlex.

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  8. Glucocorticoid-Induced Ocular Hypertension and Glaucoma.Clinical ophthalmology (Auckland, N.Z.) · 2024
    Review
  9. Identification of the function ofTranslational cancer research · 2023
    Article
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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

3 authors at 2 institutions in 1 country.

Cachétne S X BarrettCenter for Cancer Research and Therapeutic Development, Clark Atlanta University, Atlanta, Georgia.
Ana C MillenaCenter for Cancer Research and Therapeutic Development, Clark Atlanta University, Atlanta, Georgia.
Shafiq A KhanCenter for Cancer Research and Therapeutic Development, Clark Atlanta University, Atlanta, Georgia.
Clark Atlanta University · USCenter for Cancer Research · US

Funding

TRAINNING COREP20MD002285 · NIMHD · CLARK ATLANTA UNIVERSITY · PI KHAN, SHAFIQ A · 2007 to 2016
$10.9M
Technologies/Resources for Core LaboratoriesG12MD007590 · NIMHD · CLARK ATLANTA UNIVERSITY · PI KHAN, SHAFIQ A · 2012 to 2018
$7.6M
NIMHD NIH HHS G12 MD007590NIMHD NIH HHS P20 MD002285
6 · The paper itself

Abstract

backgroundActivator Protein-1 (AP-1) family (cJun, JunB, JunD, cFos, FosB, Fra1, and Fra2) plays a central role in the transcriptional regulation of many genes that are associated with cell proliferation, differentiation, migration, metastasis, and survival. Many oncogenic signaling pathways converge at the AP-1 transcription complex. Transforming growth factor beta (TGF-β) is a multifunctional regulatory cytokine that regulates many aspects of cellular function, including cellular proliferation, differentiation, migration, apoptosis, adhesion, angiogenesis, immune surveillance, and survival.

methodsThis study investigated, the role of FOS proteins in TGF-β signaling in prostate cancer cell proliferation, migration, and invasion. Steady state expression levels of FOS mRNA and proteins were determined using RT-PCR and western blotting analyses. DU145 and PC3 prostate cancer cells were exposed to TGF-β1 at varying time and dosage, RT-PCR, western blot, and immunofluorescence analyses were used to determine TGF-β1 effect on FOS mRNA and protein expression levels as well as FosB subcellular localization. Transient silencing of FosB protein was used to determine its role in cell proliferation, migration, and invasion.

resultsOur data show that FOS mRNA and proteins were differentially expressed in human prostate epithelial (RWPE-1) and prostate cancer cell lines (LNCaP, DU145, and PC3). TGF-β1 induced the expression of FosB at both the mRNA and protein levels in DU145 and PC3 cells, whereas cFos and Fra1 were unaffected. Immunofluorescence analysis showed an increase in the accumulation of FosB protein in the nucleus of PC3 cells after treatment with exogenous TGF-β1. Selective knockdown of endogenous FosB by specific siRNA did not have any effect on cell proliferation in PC3 and DU145 cells. However, basal and TGF-β1- and EGF-induced cell migration was significantly reduced in DU145 and PC3 cells lacking endogenous FosB. TGF-β1- and EGF-induced cell invasion were also significantly decreased after FosB knockdown in PC3 cells.

conclusionOur data suggest that FosB is required for migration and invasion in prostate cancer cells. We also conclude that TGF-β1 effect on prostate cancer cell migration and invasion may be mediated through the induction of FosB. Prostate 77:72-81, 2017. © 2016 Wiley Periodicals, Inc.

Indexed as

Cell Line, TumorCell MovementCell ProliferationDose-Response Relationship, DrugHEK293 CellsHumansMaleNeoplasm InvasivenessProstatic NeoplasmsProto-Oncogene Proteins c-fosTransforming Growth Factor betaFOSB protein, humanProto-Oncogene Proteins c-fosTransforming Growth Factor betaAP-1cell invasioncell migrationFosBprostate cancerTGF-β

Identifiers

PMID27604827
PMCPMC5286811
OpenAlexW2520343687

What OpenQuestion holds

Textmetadata
LicenceTDM
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.