Evidence map›Paper›PMID 29348460›Full record

ArticleOncogene2018

FYN promotes mesenchymal phenotypes of basal type breast cancer cells through STAT5/NOTCH2 signaling node.

Ga-Hang Lee, Ki-Chun Yoo, Yoojeong An, Hae-June Lee, Minyoung Lee, Nizam Uddin, Min-Jung Kim, In-Gyu Kim, Yongjoon Suh, Su-Jae Lee

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed, 2 pooled it
4.0field-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

41 citing papers in PubMed, 2 syntheses or guidelines pooled it, 68 citations in OpenAlex.

  1. Pooled it
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  10. Advances in the expression and function of Fyn in different human tumors.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2023
    Review
  11. Review
  12. FYN/TOPK/HSPB1 axis facilitates the proliferation and metastasis of gastric cancer.Journal of experimental & clinical cancer research : CR · 2023
    Article
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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 5 institutions in 2 countries.

Ga-Hang LeeDepartment of Life Science, Research Institute for Natural Sciences, Hanyang University, Seoul, Korea.
Ki-Chun YooDepartment of Life Science, Research Institute for Natural Sciences, Hanyang University, Seoul, Korea.
Yoojeong AnDepartment of Life Science, Research Institute for Natural Sciences, Hanyang University, Seoul, Korea.
Hae-June LeeDivision of Radiation Effect, Korea Institute of Radiological and Medical Sciences, Seoul, Korea.
Minyoung LeeDivision of Radiation Effect, Korea Institute of Radiological and Medical Sciences, Seoul, Korea.
Nizam UddinDepartment of Life Science, Research Institute for Natural Sciences, Hanyang University, Seoul, Korea.
Min-Jung KimLaboratory of Radiation Exposure & Therapeutics, National Radiation Emergency Medical Center, Korea Institute of Radiological and Medical Sciences, Seoul, Korea.
In-Gyu KimDepartment of Radiation Biology, Environmental Radiation Research Group, Korea Atomic Energy Research Institute, Daejeon, Republic of Korea.
Yongjoon SuhDepartment of Life Science, Research Institute for Natural Sciences, Hanyang University, Seoul, Korea. hiswork@hanmail.net.
Su-Jae LeeDepartment of Life Science, Research Institute for Natural Sciences, Hanyang University, Seoul, Korea. sj0420@hanyang.ac.kr.
Hanyang University · KRKorea Institute of Radiological and Medical Sciences · KRCentre of Excellence in Molecular Biology · PKKorea Atomic Energy Research Institute · KRSamsung Medical Center · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Basal type breast cancer is the most aggressive and has mesenchymal features with a high metastatic ability. However, the signaling node that determines the basal type features in breast cancer remains obscure. Here, we report that FYN among SRC family kinases is required for the maintenance of basal type breast cancer subtype. Importantly, FYN enhanced NOTCH2 activation in basal type breast cancer cells through STAT5-mediated upregulation of Jagged-1 and DLL4 NOTCH ligands, thereby contributed to mesenchymal phenotypes. In addition, we found that high levels of FYN persist in basal type breast cancer cells by a positive feedback loop between FYN and STAT5. FYN interacted directly with STAT5 and increased p-STAT5 that further acts as a transcription factor for FYN. Taken together, our findings demonstrate a pivotal role of FYN and its downstream effectors in maintaining the basal type features in breast cancer.

Indexed as

AnimalsBreast NeoplasmsCell Line, TumorEpithelial-Mesenchymal TransitionFemaleHumansMCF-7 CellsMiceMice, Inbred BALB CMice, Inbred NODMice, NudeMice, SCIDPhenotypeProto-Oncogene Proteins c-fynReceptor, Notch2Signal TransductionFYN protein, humanNOTCH2 protein, humanProto-Oncogene Proteins c-fynReceptor, Notch2STAT5A protein, humanSTAT5 Transcription FactorTumor Suppressor Proteins

Identifiers

PMID29348460
OpenAlexW2801253660

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.