Evidence map›Paper›PMID 21076047›Full record

ArticleMolecular cancer research : MCR2011

Loss of PTEN permits CXCR4-mediated tumorigenesis through ERK1/2 in prostate cancer cells.

Mahandranauth A Chetram, Valerie Odero-Marah, Cimona V Hinton

Open access · bronzeAbstract read
In one paragraph

Article in Molecular cancer research : MCR, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
2.3field-weighted citation impact, top 12% 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, 59 citations in OpenAlex.

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  17. OverexpressingOncotarget · 2018
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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 1 institution in 1 country.

Mahandranauth A ChetramClark Atlanta University, Center for Cancer Research and Therapeutic Development, 223 James P. Brawley Drive, SW, Atlanta, GA 30314, USA.
Valerie Odero-Marah
Cimona V Hinton
Clark Atlanta University · US

Funding

THEORY OF PLANNED BEHAVIOR VS ETHNICITY /PHYSICAL ACTIVIG12RR003062 · NCRR · CLARK ATLANTA UNIVERSITY · PI BROWN, CARLTON B · 1985 to 2011
$15.5M
Research Initiative for Scientific Enhancement (RISE)R25GM060414 · NIGMS · CLARK ATLANTA UNIVERSITY · PI MUSEY, PAUL I. · 1999 to 2020
$13.7M
TRAINNING COREP20MD002285 · NIMHD · CLARK ATLANTA UNIVERSITY · PI CHAUDHARY, JAIDEEP · 2007 to 2016
$10.9M
The Regulatory Role of PTEN on CXCR4-mediated Metastasis in Prostate Cancer CellsF31CA153908 · NCI · CLARK ATLANTA UNIVERSITY · PI CHETRAM, MAHANDRANAUTH ANAND · 2011 to 2011
$29k
NCI NIH HHS F31 CA153908NCRR NIH HHS 2G12RR003062-22NCRR NIH HHS G12 RR003062NIGMS NIH HHS 5R25GM060414NIGMS NIH HHS R25 GM060414NIMHD NIH HHS 1P20MD002285NIMHD NIH HHS P20 MD002285
6 · The paper itself

Abstract

Loss of PTEN is frequently observed in androgen-independent prostate cancer, resulting in the deregulation of metastatic events. SDF1α activation of CXCR4 induces signaling pathways that have been implicated in prostate metastasis and progression to an advanced disease. The pathways of CXCR4 and PTEN converge, leading to the promotion and regulation of tumorigenesis, respectively. However, loss of PTEN may permit CXCR4 to progress prostate cancer to an advanced disease. In the present study, we investigated the involvement of PTEN in CXCR4-mediated tumorigenesis. When screening advanced metastatic prostate cancer cell lines for PTEN, we observed a loss of expression in PC3 and LNCaP cells whereas Du145 expressed wild-type PTEN. All three cell lines were positive for surface expression of CXCR4. Reconsitution of PTEN induced a mesenchymal to epithelial like morphologic change and inhibited CXCR4-mediated migration and proliferation in PC3 cells. Downregulation of PTEN by siRNA enhanced the CXCR4-mediated migratory behavior of Du145 cells. By Western blot analysis, we observed that PTEN inhibited basal AKT phosphorylation but not ERK1/2 phosphorylation in PTEN-expressing cells. Upon CXCR4 stimulation, PTEN inhibited ERK1/2 phosphorylation but not phosphorylation of AKT. The CXCR4-mediated migration of PC3 cells was through the ERK1/2 pathway, as confirmed by chemical inhibitors. On the basis of these studies, we suggest that loss of PTEN permits CXCR4-mediated functions in prostate cancer cells through the ERK1/2 pathway. Antagonizing CXCR4 and downstream signaling cascades may provide an efficient approach for treating patients with advanced prostate cancer when hormone therapy fails to the stop the growth and containment of tumors.

Indexed as

Blotting, WesternCell Line, TumorCell MovementCell ProliferationGene Expression Regulation, NeoplasticGreen Fluorescent ProteinsHEK293 CellsHumansMaleMicroscopy, FluorescenceMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3PhosphorylationProstatic NeoplasmsPTEN PhosphohydrolaseReceptors, CXCR4CXCR4 protein, humanGreen Fluorescent ProteinsMAPK1 protein, humanMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3PTEN PhosphohydrolasePTEN protein, humanReceptors, CXCR4

Identifiers

PMID21076047
PMCPMC3443870
OpenAlexW2130263407

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.