Evidence map›Paper›PMID 26494555›Full record

ArticleCancer gene therapy2015

HuR-targeted nanotherapy in combination with AMD3100 suppresses CXCR4 expression, cell growth, migration and invasion in lung cancer.

R Muralidharan, J Panneerselvam, A Chen, Y D Zhao, A Munshi, R Ramesh

Open access · bronzeAbstract read
In one paragraph

Article in Cancer gene therapy, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
2.6field-weighted citation impact, top 10% 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

33 citing papers in PubMed, 46 citations in OpenAlex.

  1. Article
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  16. Article
  17. The Effects of the CXCR4 Antagonist, AMD3465, on Human Retinal Vascular Endothelial Cells (hRVECs) in a High Glucose Model of Diabetic Retinopathy.Medical science monitor : international medical journal of experimental and clinical research · 2019
    Article
  18. Article
  19. Targeting CXCL12/CXCR4 Axis in Tumor Immunotherapy.Current medicinal chemistry · 2019
    Review
  20. Article
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 1 institution in 1 country.

R MuralidharanDepartment of Pathology, Stanton L. Young Biomedical Research Center, The University of Oklahoma Health Sciences Center, Oklahoma City, OK, USA.
J PanneerselvamDepartment of Pathology, Stanton L. Young Biomedical Research Center, The University of Oklahoma Health Sciences Center, Oklahoma City, OK, USA.
A ChenDepartment of Biostatistics and Epidemiology, The University of Oklahoma Health Sciences Center, Oklahoma City, OK, USA.
Y D ZhaoStephenson Cancer Center, The University of Oklahoma Health Sciences Center, Oklahoma City, OK, USA.
A MunshiStephenson Cancer Center, The University of Oklahoma Health Sciences Center, Oklahoma City, OK, USA.
R RameshDepartment of Pathology, Stanton L. Young Biomedical Research Center, The University of Oklahoma Health Sciences Center, Oklahoma City, OK, USA.
University of Oklahoma Health Sciences Center · US

Funding

TUMOR RESISTANCE MECHANISMS TO ANTI-VEGF THERAPY IN PROSTATE CANCER (Sukyung Woo)P20GM103639 · NIGMS · UNIVERSITY OF OKLAHOMA HLTH SCIENCES CTR · PI DHANASEKARAN, DANNY N. · 2012 to 2022
$21.3M
HuR Targeted Nanotherapy for Lung CancerR01CA167516 · NCI · UNIVERSITY OF OKLAHOMA HLTH SCIENCES CTR · PI RAMESH, RAJAGOPAL · 2013 to 2017
$1.9M
NCI NIH HHS R01 CA167516NIGMS NIH HHS P20 GM103639
6 · The paper itself

Abstract

The CXCR4 chemokine receptor has an important role in cancer cell metastasis. The CXCR4 antagonist, AMD3100, has limited efficacy in controlling metastasis. HuR, an RNA-binding protein, regulates CXCR4 in cancer cells. We therefore investigated whether targeting HuR using a siRNA-based nanoparticle plus AMD3100 would suppress CXCR4 and inhibit lung cancer metastasis. We treated human H1299 lung cancer cells with HuR-specific siRNA contained in a folate-targeted lipid nanoparticle (HuR-FNP) plus AMD3100, and compared this with AMD3100 alone, HuR-FNP alone and no treatment. HuR-FNP plus AMD3100 treatment produced a G1 phase cell cycle arrest and reduced cell viability above and beyond the effects of AMD3100 alone. HuR and CXCR4 mRNA and protein expression levels were markedly reduced in all treatment groups. Phosphorylated (p) AKT(S473) protein was also reduced. P27 protein expression increased with HuR-FNP and combination treatment. Promoter-based reporter studies showed that the combination inhibited CXCR4 promoter activity more than did either treatment alone. Cell migration and invasion was significantly reduced with all treatments; the combination provided the most inhibition. Reduced matrix metalloprotease (MMP)-2 and -9 expression was associated with reduced invasion in all treatment groups. Thus, we found that combined HuR and CXCR4 targeting effectively controlled lung cancer metastasis.

Indexed as

Antineoplastic AgentsBenzylaminesCell MovementCell ProliferationCombined Modality TherapyCyclamsDown-RegulationELAV-Like Protein 1Heterocyclic CompoundsHumansLung NeoplasmsNanoparticlesNeoplasm InvasivenessReceptors, CXCR4RNA, Small InterferingAntineoplastic AgentsBenzylaminesCXCR4 protein, humanCyclamsELAVL1 protein, humanELAV-Like Protein 1Heterocyclic CompoundsplerixaforReceptors, CXCR4RNA, Small Interfering

Identifiers

PMID26494555
PMCPMC4679684
OpenAlexW2176078674

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.