Evidence map›Paper›PMID 26515594›Full record

ArticleOncotarget2015

Induction of metastatic potential by TrkB via activation of IL6/JAK2/STAT3 and PI3K/AKT signaling in breast cancer.

Min Soo Kim, Won Sung Lee, Joon Jeong, Seong-Jin Kim, Wook Jin

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 67 papers.

0numbers the graph read from it
0cells of the map it votes in
67citing papers in PubMed
6.0field-weighted citation impact, top 2% 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

67 citing papers in PubMed, 114 citations in OpenAlex.

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  9. BDNF and its signaling in cancer.Journal of cancer research and clinical oncology · 2023
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  18. FABP4 activates the JAK2/STAT2 pathway via Rap1a in the homocysteine-induced macrophage inflammatory response in ApoELaboratory investigation; a journal of technical methods and pathology · 2022
    Article
  19. Article
  20. Article

7 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

5 authors at 3 institutions in 1 country.

Min Soo KimLaboratory of Molecular Disease and Cell Regulation, Department of Molecular Medicine, School of Medicine, Gachon University, Incheon 406-840, Korea.
Won Sung LeeLaboratory of Molecular Disease and Cell Regulation, Department of Molecular Medicine, School of Medicine, Gachon University, Incheon 406-840, Korea.
Joon JeongDepartment of Surgery, Kangnam Severance Hospital, Yonsei University, Kangnam, Seoul 146-92, Korea.
Seong-Jin KimCHA Cancer Institute, CHA University, Seongnam-si, Kyunggi-do 463-400, Korea.
Wook JinLaboratory of Molecular Disease and Cell Regulation, Department of Molecular Medicine, School of Medicine, Gachon University, Incheon 406-840, Korea.
Gachon University · KRCHA University · KRGangnam Severance Hospital · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In metastatic breast cancers, the acquisition of metastatic ability, which leads to clinically incurable disease and poor survival, has been associated with acquisition of epithelial-mesenchymal transition (EMT) program and self-renewing trait (CSCs) via activation of PI3K/AKT and IL6/JAK2/STAT3 signaling pathways. We found that TrkB is a key regulator of PI3K/AKT and JAK/STAT signal pathway-mediated tumor metastasis and EMT program. Here, we demonstrated that TrkB activates AKT by directly binding to c-Src, leading to increased proliferation. Also, TrkB increases Twist-1 and Twist-2 expression through activation of JAK2/STAT3 by inducing c-Src-JAK2 complex formation. Furthermore, TrkB in the absence of c-Src binds directly to JAK2 and inhibits SOCS3-mediated JAK2 degradation, resulting in increased total JAK2 and STAT3 levels, which subsequently leads to JAK2/STAT3 activation and Twist-1 upregulation. Additionally, activation of the JAK2/STAT3 pathway via induction of IL-6 secretion by TrkB enables induction of activation of the EMT program via induction of STAT3 nuclear translocation. These observations suggest that TrkB is a promising target for future intervention strategies to prevent tumor metastasis, EMT program and self-renewing trait in breast cancer.

Indexed as

AnimalsBlotting, WesternBreast NeoplasmsCell LineCell Line, TumorDogsGene Expression Regulation, NeoplasticHEK293 CellsHumansInterleukin-6Janus Kinase 2Madin Darby Canine Kidney CellsMembrane GlycoproteinsMice, Inbred BALB CMice, NudeNeoplasm MetastasisInterleukin-6JAK2 protein, humanJanus Kinase 2Membrane GlycoproteinsPhosphatidylinositol 3-KinasesProtein-Tyrosine KinasesProto-Oncogene Proteins c-aktReceptor, trkBSTAT3 Transcription Factortropomyosin-related kinase-B, humanTwist-Related Protein 1epithelial-mesenchymal transition (EMT)IL-6/JAK2/STAT3 pathwaymetastasis and tumorigenicityPI3K/AKT pathwayTrkB

Identifiers

PMID26515594
PMCPMC4741886
OpenAlexW2174136167

What OpenQuestion holds

Textmetadata
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.