Evidence map›Paper›PMID 25775124›Full record

ArticlePloS one2015

IL-24 inhibits lung cancer cell migration and invasion by disrupting the SDF-1/CXCR4 signaling axis.

Janani Panneerselvam, Jiankang Jin, Manish Shanker, Jason Lauderdale, Jonathan Bates, Qi Wang, Yan D Zhao, Stephen J Archibald, Timothy J Hubin, Rajagopal Ramesh

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed
3.6field-weighted citation impact, top 5% 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

46 citing papers in PubMed, 67 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

10 authors at 4 institutions in 2 countries.

Janani PanneerselvamDepartment of Pathology, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma, United States of America; Stephenson Cancer Center, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma, United States of America.
Jiankang JinDepartment of Thoracic and Cardiovascular Surgery, The University of Texas MD Anderson Cancer Center, Houston, Texas, United States of America.
Manish ShankerDepartment of Thoracic and Cardiovascular Surgery, The University of Texas MD Anderson Cancer Center, Houston, Texas, United States of America.
Jason LauderdaleDepartment of Pathology, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma, United States of America; Stephenson Cancer Center, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma, United States of America.
Jonathan BatesDepartment of Pathology, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma, United States of America; Stephenson Cancer Center, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma, United States of America.
Qi WangDepartment of Pathology, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma, United States of America; Stephenson Cancer Center, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma, United States of America.
Yan D ZhaoDepartment of Pathology, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma, United States of America; Department of Biostatistics and Epidemiology, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma, United States of America.
Stephen J ArchibaldDepartment of Chemistry, The University of Hull, Hull, United Kingdom.
Timothy J HubinStephenson Cancer Center, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma, United States of America; Department of Chemistry, Southwestern Oklahoma State University, Weatherford, Oklahoma, United States of America.
Rajagopal RameshDepartment of Pathology, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma, United States of America; Stephenson Cancer Center, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma, United States of America; Graduate Program in Biomedical Sciences, Oklahoma City, Oklahoma, United States of America.
University of Oklahoma Health Sciences Center · USThe University of Texas MD Anderson Cancer Center · USUniversity of Hull · GBWeatherford (United States) · 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
NIGMS NIH HHS P20 GM103639
6 · The paper itself

Abstract

backgroundThe stromal cell derived factor (SDF)-1/chemokine receptor (CXCR)-4 signaling pathway plays a key role in lung cancer metastasis and is molecular target for therapy. In the present study we investigated whether interleukin (IL)-24 can inhibit the SDF-1/CXCR4 axis and suppress lung cancer cell migration and invasion in vitro. Further, the efficacy of IL-24 in combination with CXCR4 antagonists was investigated.

methodsHuman H1299, A549, H460 and HCC827 lung cancer cell lines were used in the present study. The H1299 lung cancer cell line was stably transfected with doxycycline-inducible plasmid expression vector carrying the human IL-24 cDNA and used in the present study to determine the inhibitory effects of IL-24 on SDF-1/CXCR4 axis. H1299 and A549 cell lines were used in transient transfection studies. The inhibitory effects of IL-24 on SDF1/CXCR4 and its downstream targets were analyzed by quantitative RT-PCR, western blot, luciferase reporter assay, flow cytometry and immunocytochemistry. Functional studies included cell migration and invasion assays. PRINCIPAL

findingsEndogenous CXCR4 protein expression levels varied among the four human lung cancer cell lines. Doxycycline-induced IL-24 expression in the H1299-IL24 cell line resulted in reduced CXCR4 mRNA and protein expression. IL-24 post-transcriptionally regulated CXCR4 mRNA expression by decreasing the half-life of CXCR4 mRNA (>40%). Functional studies showed IL-24 inhibited tumor cell migration and invasion concomitant with reduction in CXCR4 and its downstream targets (pAKTS473, pmTORS2448, pPRAS40T246 and HIF-1α). Additionally, IL-24 inhibited tumor cell migration both in the presence and absence of the CXCR4 agonist, SDF-1. Finally, IL-24 when combined with CXCR4 inhibitors (AMD3100, SJA5) or with CXCR4 siRNA demonstrated enhanced inhibitory activity on tumor cell migration.

conclusionsIL-24 disrupts the SDF-1/CXCR4 signaling pathway and inhibits lung tumor cell migration and invasion. Additionally, IL-24, when combined with CXCR4 inhibitors exhibited enhanced anti-metastatic activity and is an attractive therapeutic strategy for lung metastasis.

Indexed as

BenzylaminesCarcinoma, Non-Small-Cell LungCell Line, TumorCell MovementChemokine CXCL12CyclamsDrug SynergismGene ExpressionGene Expression Regulation, NeoplasticHeterocyclic CompoundsHumansInterleukin-24InterleukinsLung NeoplasmsProto-Oncogene Proteins c-aktReceptors, CXCR4BenzylaminesChemokine CXCL12CyclamsHeterocyclic CompoundsInterleukin-24InterleukinsplerixaforProto-Oncogene Proteins c-aktReceptors, CXCR4RNA, Small InterferingTOR Serine-Threonine Kinases

Identifiers

PMID25775124
PMCPMC4361489
OpenAlexW2053699199

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.