Evidence map›Paper›PMID 25327819›Full record

ArticleThe Prostate2015

Interferon inducible antiviral MxA is inversely associated with prostate cancer and regulates cell cycle, invasion and Docetaxel induced apoptosis.

Shanora G Brown, Ashley E Knowell, Aisha Hunt, Divya Patel, Sushma Bhosle, Jaideep Chaudhary

Abstract read
In one paragraph

Article in The Prostate, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.7field-weighted citation impact, top 16% 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

17 citing papers in PubMed, 32 citations in OpenAlex.

  1. Article
  2. Effects ofMicroorganisms · 2021
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  8. Exosomal αvβ6 integrin is required for monocyte M2 polarization in prostate cancer.Matrix biology : journal of the International Society for Matrix Biology · 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

6 authors at 2 institutions in 1 country.

Shanora G BrownDepartment of Biology, South Carolina State University, Orangeburg, South Carolina.
Ashley E Knowell
Aisha Hunt
Divya Patel
Sushma Bhosle
Jaideep Chaudhary
Clark Atlanta University · USSouth Carolina State University · US

Funding

THEORY OF PLANNED BEHAVIOR VS ETHNICITY /PHYSICAL ACTIVIG12RR003062 · NCRR · CLARK ATLANTA UNIVERSITY · PI BROWN, CARLTON B · 1985 to 2011
$15.5M
TRAINNING COREP20MD002285 · NIMHD · CLARK ATLANTA UNIVERSITY · PI CHAUDHARY, JAIDEEP · 2007 to 2016
$10.9M
Technologies/Resources for Core LaboratoriesG12MD007590 · NIMHD · CLARK ATLANTA UNIVERSITY · PI KHAN, SHAFIQ A · 2012 to 2018
$7.6M
NCRR NIH HHS G12 RR003062NCRR NIH HHS G12RR03062NIMHD NIH HHS G12 MD007590NIMHD NIH HHS P20 MD002285NIMHD NIH HHS P20MD002285-01
6 · The paper itself

Abstract

backgroundThe interferon inducible Myxovirus (influenza virus) resistance A (MxA) is considered as a key mediator of the interferon-induced antiviral response. Mx proteins contain the typical GTP-binding motif and show significant homology to dynamin family of GTPases. Strong interaction of MxA with tubulin suggests that Mx proteins could be involved in mitosis. Studies have shown that MxA inhibit tumor motility/metastasis and virus induced apoptosis. However, the clear association between MxA expression and cancer remains unknown. Meta-analysis suggested that MxA expression was inversely correlated with prostate cancer (PCa). In this study, we demonstrate the expression MxA in PCa and its functional significance on the cancer phenotype.

methodsThe expression of MxA protein in prostate cancer was examined by immuno-histochemistry. MxA was knocked down (shMxA) or over-expressed (pMxA) in DU145 or LNCaP PCa cell lines respectively. These cell lines were used to study proliferation, apoptosis, invasion, migration, and anchorage independent growth. Co-localization of MxA with tubulin was performed by immuno-cytochemistry following Docetaxel treatment.

resultsThe expression of MxA protein was significantly decreased in PCa as compared to the normal tissues. DU145 cells lacking MxA (DU145 + chMxA) showed significant increase in proliferation, associated with decreased expression of CDKN1A and B. Increased migration, anchorage independent growth in DU145 + shMxA cells was associated with increased MMP13 expression. Tubulin organization was also dependent on MxA expression. Tubulin polymerizing agents such as Docetaxel was less effective in promoting apoptosis in cells lacking MxA due to altered tubulin organization. Gain of MxA expression in LNCaP cells (LNCaP + pMxA) resulted in cell cycle arrest that was associated with increased expression of CDKN1A. MxA expression was also down-regulated by dihydrotestosterone in LNCaP cells.

conclusionsMxA expression is inversely correlated with prostate cancer. Down-regulation of MxA in LNCaP cells by DHT suggests that MxA could play a significant role in disease progression. Loss of MxA expression results in increased metastasis and decreased sensitivity to Docetaxel suggesting that MxA expression could determine the outcome of chemo-therapeutic treatment. Additional studies will be required to fully establish the cross-talk between androgen receptor-IFN pathway in regulating MxA expression in the normal prostate and prostate cancer. Prostate 75:266-279, 2015. © 2014 Wiley Periodicals, Inc.

Indexed as

ApoptosisCell CycleCell DivisionCell Line, TumorDocetaxelHumansMaleMyxovirus Resistance ProteinsNeoplasm InvasivenessProstatic NeoplasmsTaxoidsTubulinDocetaxelMX1 protein, humanMyxovirus Resistance ProteinsTaxoidsTubulinDocetaxelMxAprostate cancer

Identifiers

PMID25327819
PMCPMC4293202
OpenAlexW1530818192

What OpenQuestion holds

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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.