Evidence map›Paper›PMID 23955082›Full record

ArticleOncogene2014

Inflammatory lipid sphingosine-1-phosphate upregulates C-reactive protein via C/EBPβ and potentiates breast cancer progression.

E-S Kim, Y Cha, M Ham, J Jung, S G Kim, S Hwang, R Kleemann, A Moon

Open access · bronzeAbstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
1.5field-weighted citation impact, top 18% 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

26 citing papers in PubMed, 43 citations in OpenAlex.

  1. Review
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  6. Sphingolipids in mitochondria-from function to disease.Frontiers in cell and developmental biology · 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

8 authors at 4 institutions in 2 countries.

E-S KimCollege of Pharmacy, Duksung Women's University, Seoul, Korea.
Y ChaCollege of Pharmacy, Duksung Women's University, Seoul, Korea.
M HamCollege of Pharmacy, Duksung Women's University, Seoul, Korea.
J JungCollege of Pharmacy, Duksung Women's University, Seoul, Korea.
S G KimCollege of Pharmacy and Research Institute of Pharmaceutical Sciences Seoul National University, Seoul, Korea.
S HwangCollege of Medicine, Hanyang University, Seoul, Korea.
R KleemannMetabolic Health Research, TNO, CK Leiden, The Netherlands.
A MoonCollege of Pharmacy, Duksung Women's University, Seoul, Korea.
Duksung Women's University · KRHanyang University · KRNetherlands Metabolomics Centre · NLSeoul National University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

A crucial role of the inflammatory lipid sphingosine-1-phosphate (S1P) in breast cancer aggressiveness has been reported. Recent clinical studies have suggested that C-reactive protein (CRP) has a role in breast cancer development. However, limited information is available on the molecular basis for the expression of CRP and its functional significance in breast cell invasion. The present study aimed to elucidate the molecular link between S1P and CRP during the invasive process of breast epithelial cells. This is the first report showing that transcription of CRP was markedly activated by S1P in breast cells. Our data suggest that not only S1P treatment but also the endogenously produced S1P may upregulate CRP in breast carcinoma cells. Transcription factors CCAAT/enhancer-binding protein beta and c-fos were required for S1P-induced CRP expression. Coupling of S1P3 to heterotrimeric Gαq triggered the expression of CRP, utilizing signaling pathways involving reactive oxygen species (ROS), Ca(2+) and extracellular signal-related kinases (ERKs). S1P-induced CRP expression was crucial for the transcriptional activation of matrix metalloproteinase-9 through ERKs, ROS and c-fos, leading to breast cell invasion. Using a xenograft mice tumor model, we demonstrated that S1P induced CRP expression both in vitro and in vivo. Taken together, our findings have revealed a molecular basis for S1P-induced transcriptional activation of CRP and its functional significance in the acquisition of the invasive phenotype of human breast epithelial cells under inflammatory conditions. Our findings may provide useful information on the identification of useful therapeutic targets for inflammatory breast cancer.

Indexed as

Disease ProgressionAnimalsBreast NeoplasmsCalciumCCAAT-Enhancer-Binding Protein-betaCell Line, TumorC-Reactive ProteinEnzyme ActivationExtracellular Signal-Regulated MAP KinasesFemaleHumansInflammationLysophospholipidsMatrix Metalloproteinase 9MiceNeoplasm InvasivenessCalciumCCAAT-Enhancer-Binding Protein-betaC-Reactive ProteinExtracellular Signal-Regulated MAP KinasesLysophospholipidsMatrix Metalloproteinase 9Proto-Oncogene Proteins c-fosReactive Oxygen SpeciesSphingosinesphingosine 1-phosphate

Identifiers

PMID23955082
OpenAlexW2098218803

What OpenQuestion holds

Textmetadata
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.