Evidence map›Paper›PMID 24990945›Full record

ArticleThe Journal of biological chemistry2014

Ras promotes transforming growth factor-β (TGF-β)-induced epithelial-mesenchymal transition via a leukotriene B4 receptor-2-linked cascade in mammary epithelial cells.

Hyunju Kim, Jung-A Choi, Jae-Hong Kim

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
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

31 citing papers in PubMed, 45 citations in OpenAlex.

  1. Article
  2. Article
  3. Two distinct forms of human BLT2: long-form and short-form BLT2.Frontiers in cell and developmental biology · 2023
    Review
  4. Review
  5. Article
  6. Review
  7. Article
  8. Article
  9. Ras Signaling in Breast Cancer.Advances in experimental medicine and biology · 2021
    Article
  10. Article
  11. Leukotrienes in Tumor-Associated Inflammation.Frontiers in pharmacology · 2020
    Review
  12. Review
  13. Article
  14. Review
  15. RAS as Supporting Actor in Breast Cancer.Frontiers in oncology · 2019
    Review
  16. Article
  17. Review
  18. Review
  19. Article
  20. Review
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

3 authors at 1 institution in 1 country.

Hyunju KimFrom the College of Life Sciences and Biotechnology, Korea University, Seoul 136-701, Korea.
Jung-A ChoiFrom the College of Life Sciences and Biotechnology, Korea University, Seoul 136-701, Korea.
Jae-Hong KimFrom the College of Life Sciences and Biotechnology, Korea University, Seoul 136-701, Korea jhongkim@korea.ac.kr.
Korea University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Inflammation and inflammatory mediators are inextricably linked with epithelial-mesenchymal transition (EMT) through complex pathways in the tumor microenvironment. However, the mechanism by which inflammatory mediators, such as the lipid inflammatory mediators, eicosanoids, contribute to EMT is largely unknown. In the present study we observed that BLT2, leukotriene B4 receptor-2, is markedly up-regulated by oncogenic Ras and promotes EMT in response to transforming growth factor-β (TGF-β) in mammary epithelial cells. Blockade of BLT2 by the BLT2 inhibitor LY255283 or by siRNA reduced EMT induced by Ras in the presence of TGF-β. In addition, stimulation of BLT2 by the addition of a BLT2 ligand, such as leukotriene B4, restored EMT in the presence of TGF-β in human immortalized mammary epithelial MCF-10A cells. We further searched BLT2 downstream components and identified reactive oxygen species and nuclear factor κB as critical components that contribute to EMT. Taken together, these results demonstrate for the first time that a BLT2-linked inflammatory pathway contributes to EMT. This provides valuable insight into the mechanism of EMT in mammary epithelial cells. In addition, considering the implications of EMT with the stemness of cancer cells, our finding may contribute to a better understanding of tumor progression.

Indexed as

Breast NeoplasmsCell LineEpithelial-Mesenchymal TransitionFemaleHumansMammary Glands, HumanNADPH Oxidase 1NADPH OxidasesNF-kappa BProto-Oncogene Proteins p21(ras)Reactive Oxygen SpeciesReceptors, Leukotriene B4RNA, Small InterferingSignal TransductionTetrazolesTransforming Growth Factor betaHRAS protein, humanLTB4R2 protein, humanLY 255283NADPH Oxidase 1NADPH OxidasesNF-kappa BNOX1 protein, humanProto-Oncogene Proteins p21(ras)Reactive Oxygen SpeciesReceptors, Leukotriene B4RNA, Small InterferingTetrazolesTransforming Growth Factor betaBLT2Epithelial-Mesenchymal Transition (EMT)NADPH OxidaseNF-κB (NF-KB)Ras ProteinReactive Oxygen Species (ROS)TGF-β

Identifiers

PMID24990945
PMCPMC4139228
OpenAlexW1979259332

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.