Evidence map›Paper›PMID 24376747›Full record

ArticlePloS one2013

CXCR2-driven ovarian cancer progression involves upregulation of proinflammatory chemokines by potentiating NF-κB activation via EGFR-transactivated Akt signaling.

Yuan-Lin Dong, Syeda M Kabir, Eun-Sook Lee, Deok-Soo Son

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed, 1 pooled it
3.0field-weighted citation impact, top 8% 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

35 citing papers in PubMed, 1 synthesis or guideline pooled it, 62 citations in OpenAlex.

  1. Pooled it
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  6. Therapeutic inhibition of CXCR1/2: where do we stand?Internal and emergency medicine · 2023
    Review
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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

4 authors at 1 institution in 1 country.

Yuan-Lin DongDepartment of Biochemistry and Cancer Biology, Meharry Medical College, Nashville, Tennessee, United States of America.
Syeda M KabirDepartment of Biochemistry and Cancer Biology, Meharry Medical College, Nashville, Tennessee, United States of America.
Eun-Sook LeeDepartment of Physiology, Meharry Medical College, Nashville, Tennessee, United States of America.
Deok-Soo SonDepartment of Biochemistry and Cancer Biology, Meharry Medical College, Nashville, Tennessee, United States of America.
Meharry Medical College · US

Funding

Meharry RCMI Program in Women's Health ResearchG12MD007586 · NIMHD · MEHARRY MEDICAL COLLEGE · PI HILDRETH, JAMES E · 2012 to 2016
$7.8M
Roles of inflammation-driven chemokines in the pathogenesis of ovarian cancerSC1AI089073 · NIAID · MEHARRY MEDICAL COLLEGE · PI SON, DEOK-SOO · 2009 to 2013
$1.8M
NCI NIH HHS SC1 089630NIAID NIH HHS SC1 AI089073NIAID NIH HHS SC1AI089073NIMHD NIH HHS G12 MD007586
6 · The paper itself

Abstract

Ovarian cancer is an inflammation-associated malignancy with a high mortality rate. CXCR2 expressing ovarian cancers are aggressive with poorer outcomes. We therefore investigated molecular mechanisms involved in CXCR2-driven cancer progression by comparing CXCR2 positive and negative ovarian cancer cell lines. Stably CXCR2 transfected SKOV-3 cells had a faster growth rate as compared to control cells transfected with empty vector. Particularly, tumor necrosis factor (TNF), abundantly expressed in ovarian cancer, enhanced cell proliferation by decreasing the G0-G1 phase in CXCR2 transfected cells. TNF increased nuclear factor-κB (NF-κB) activity to a greater degree in CXCR2 transfected cells than control cells as well as provided a greater activation of IκB. CXCR2 transfected cells expressed higher levels of its proinflammatory ligands, CXCL1/2 and enhanced more proliferation, migration, invasion and colony formation. CXCR2 positive cells also activated more EGFR, which led to higher Akt activation. Enhanced NF-κB activity in CXCR2 positive cells was reduced by a PI3K/Akt inhibitor rather than an Erk inhibitor. CXCL1 added to CXCR2 positive cells led to an increased activation of IκB. CXCL1 also led to a significantly greater number of invasive cells in CXCR2 transfected cells, which was blocked by the NF-κB inhibitor, Bay 11-7082. In addition, enhanced cell proliferation in CXCR2 positive cells was more sensitive to CXCL1 antibody or an NF-κB inhibitor. Finally, CXCR2 transfection of parental cells increased CXCL1 promoter activity via an NF-κB site. Thus augmentation of proinflammatory chemokines CXCL1/2, by potentiating NF-κB activation through EGFR-transactivated Akt, contributes to CXCR2-driven ovarian cancer progression.

Indexed as

Up-RegulationCell Line, TumorCell MovementCell ProliferationChemokine CXCL1ChemokinesDisease ProgressionErbB ReceptorsFemaleGene Expression Regulation, NeoplasticGene Knockdown TechniquesHumansLigandsNeoplasm InvasivenessNF-kappa BOvarian NeoplasmsChemokine CXCL1ChemokinesEGFR protein, humanErbB ReceptorsLigandsNF-kappa BProto-Oncogene Proteins c-aktReceptors, Interleukin-8BRNA, Small InterferingTumor Necrosis Factor-alpha

Identifiers

PMID24376747
PMCPMC3869803
OpenAlexW1992661964

What OpenQuestion holds

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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.