Evidence map›Paper›PMID 25531326›Full record

ArticleOncogene2015

Interleukin-33/ST2 axis promotes epithelial cell transformation and breast tumorigenesis via upregulation of COT activity.

J Y Kim, S-C Lim, G Kim, H J Yun, S-G Ahn, H S Choi

Abstract read
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In one paragraph

Article in Oncogene, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers.

0numbers the graph read from it
0cells of the map it votes in
61citing papers in PubMed
3.5field-weighted citation impact, top 7% 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

61 citing papers in PubMed, 90 citations in OpenAlex.

  1. Trial
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  6. Etoposide activates CD8Journal for immunotherapy of cancer · 2025
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  16. Knowledge mapping of interleukin-33: a bibliometric study.American journal of translational research · 2023
    Article
  17. Article
  18. Article
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  20. Article

1 more citing papers are in PubMed but not listed here.

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.

J Y KimCollege of Pharmacy, Chosun University, Gwangju, South Korea.
S-C LimDepartment of Pathology, School of Medicine, Chosun University, Gwangju, South Korea.
G KimCollege of Pharmacy, Chosun University, Gwangju, South Korea.
H J YunCollege of Pharmacy, Chosun University, Gwangju, South Korea.
S-G AhnDepartment of Pathology, School of Dentistry, Chosun University, Gwangju, South Korea.
H S ChoiCollege of Pharmacy, Chosun University, Gwangju, South Korea.
Chosun University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cytokines of the interleukin-1 (IL-1) family, such as IL-1α/β and IL-18, have pleiotropic activities in innate and adaptive immune responses in host defense and diseases. Insight into their biological functions helped develop novel therapeutic approaches to treat human inflammatory diseases. IL-33 is an important member of the IL-1 family of cytokines and is a ligand of the ST2 receptor, a member of the IL-1 receptor family. However, the role of the IL-33/ST2 axis in tumor growth and metastasis of breast cancer remains unclear. Here, we demonstrate that IL-33 is a critical tumor promoter during epithelial cell proliferation and tumorigenesis in the breast. IL-33 dose- and time-dependently increased Cancer Osaka Thyroid (COT) phosphorylation via ST2-COT interaction in normal epithelial and breast cancer cells. The IL-33/ST2/COT cascade induced the activation of the MEK-ERK (MEK-extracellular signal-regulated kinase), JNK-cJun (cJun N-terminal kinase-cJun) and STAT3 (signal transducer and activator of transcription 3) signaling pathways, followed by increased AP-1 and stat3 transcriptional activity. When small interfering RNAs of ST2 and COT were introduced into cells, IL-33-induced AP-1 and stat3 activity were significantly decreased, unlike that in the control cells. The inhibition of COT activity resulted in decreased IL-33-induced epithelial cell transformation, and knockdown of IL-33, ST2 and COT in breast cancer cells attenuated tumorigenicity of breast cancer cells. Consistent with these observations, ST2 levels were positively correlated with COT expression in human breast cancer. These findings provide a novel perspective on the role of the IL-33/ST2/COT signaling pathway in supporting cancer-associated inflammation in the tumor microenvironment. Therapeutic approaches that target this pathway may, therefore, effectively inhibit carcinogenesis in the breast.

Indexed as

CarcinogenesisAnimalsBreast NeoplasmsCell Line, TumorEpithelial CellsFemaleHumansInterleukin-1 Receptor-Like 1 ProteinInterleukin-33MAP Kinase Kinase KinasesMiceMice, Inbred BALB CMice, NudePhosphorylationProto-Oncogene ProteinsReceptors, Cell SurfaceIL1RL1 protein, humanIL33 protein, humanInterleukin-1 Receptor-Like 1 ProteinInterleukin-33MAP3K8 protein, humanMAP Kinase Kinase KinasesProto-Oncogene ProteinsReceptors, Cell SurfaceSTAT3 protein, humanSTAT3 Transcription Factor

Identifiers

PMID25531326
OpenAlexW2045994086

What OpenQuestion holds

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Registered trials

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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.