Evidence map›Paper›PMID 34066153›Full record

ArticleCancers2021

TrkA Interacts with and Phosphorylates STAT3 to Enhance Gene Transcription and Promote Breast Cancer Stem Cells in Triple-Negative and HER2-Enriched Breast Cancers.

Angelina T Regua, Noah R Aguayo, Sara Abu Jalboush, Daniel L Doheny, Sara G Manore, Dongqin Zhu, Grace L Wong, Austin Arrigo, Calvin J Wagner, Yang Yu and 8 more

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in Cancers, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.1field-weighted citation impact, top 20% 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

18 citing papers in PubMed, 19 citations in OpenAlex.

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  14. Pyrazolo[1,5-Molecules (Basel, Switzerland) · 2024
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

18 authors at 3 institutions in 1 country.

Angelina T ReguaDepartment of Cancer Biology, Wake Forest University School of Medicine, Winston-Salem, NC 27101, USA.ORCID 0000-0003-2595-8242
Noah R AguayoDepartment of Cancer Biology, Wake Forest University School of Medicine, Winston-Salem, NC 27101, USA.
Sara Abu JalboushDepartment of Cancer Biology, Wake Forest University School of Medicine, Winston-Salem, NC 27101, USA.
Daniel L DohenyDepartment of Cancer Biology, Wake Forest University School of Medicine, Winston-Salem, NC 27101, USA.ORCID 0000-0002-1455-3090
Sara G ManoreDepartment of Cancer Biology, Wake Forest University School of Medicine, Winston-Salem, NC 27101, USA.ORCID 0000-0003-1962-5505
Dongqin ZhuDepartment of Cancer Biology, Wake Forest University School of Medicine, Winston-Salem, NC 27101, USA.
Grace L WongDepartment of Cancer Biology, Wake Forest University School of Medicine, Winston-Salem, NC 27101, USA.ORCID 0000-0001-5986-4952
Austin ArrigoDepartment of Cancer Biology, Wake Forest University School of Medicine, Winston-Salem, NC 27101, USA.
Calvin J WagnerDepartment of Cancer Biology, Wake Forest University School of Medicine, Winston-Salem, NC 27101, USA.
Yang YuDepartment of Cancer Biology, Wake Forest University School of Medicine, Winston-Salem, NC 27101, USA.
Alexandra ThomasDepartment of Hematology and Oncology, Wake Forest University School of Medicine, Winston-Salem, NC 27101, USA.
Michael D ChanWake Forest Baptist Comprehensive Cancer Center, Wake Forest University School of Medicine, Winston-Salem, NC 27101, USA.
Jimmy RuizDepartment of Hematology and Oncology, Wake Forest University School of Medicine, Winston-Salem, NC 27101, USA.
Guangxu JinDepartment of Cancer Biology, Wake Forest University School of Medicine, Winston-Salem, NC 27101, USA.
Roy StrowdWake Forest Baptist Comprehensive Cancer Center, Wake Forest University School of Medicine, Winston-Salem, NC 27101, USA.
Peiqing SunDepartment of Cancer Biology, Wake Forest University School of Medicine, Winston-Salem, NC 27101, USA.
Jiayuh LinDepartment of Biochemistry and Molecular Biology, University of Maryland School of Medicine, Baltimore, MD 21201, USA.
Hui-Wen LoDepartment of Cancer Biology, Wake Forest University School of Medicine, Winston-Salem, NC 27101, USA.
Wake Forest University · USAtrium Health Wake Forest Baptist · USUniversity of Maryland, Baltimore · US

Funding

Tumor Tissue CoreP30CA012197 · NCI · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI Ruben A. Mesa · 1985 to 2026
$55.4M
Truncated GLI1 In GlioblastomaR01NS087169 · NINDS · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI LO, HUI-WEN · 2014 to 2018
$2.1M
Roles of tGLI1 and microRNA Network in Breast Cancer Brain MetastasisR01CA228137 · NCI · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI LO, HUI-WEN, WATABE, KOUNOSUKE · 2020 to 2025
$2.1M
Translational Oncology Training ProgramT32CA247819 · NCI · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI PARDEE, TIMOTHY SEBASTIAN, WATABE, KOUNOSUKE · 2020 to 2024
$1.4M
Foundation for the National Institutes of Health 1T32CA247819-01NCI NIH HHS P30 CA012197NCI NIH HHS R01 CA228137NCI NIH HHS T32 CA247819NIH HHS 1R01CA228137-01A1NIH HHS P30CA012197NIH HHS R01NS087169NINDS NIH HHS R01 NS087169U.S. Department of Defense W81XWH-17-1-0044U.S. Department of Defense W81XWH-19-1-0072U.S. Department of Defense W81XWH-19-1-0753U.S. Department of Defense W81XWH-20-1-0044
6 · The paper itself

Abstract

JAK2-STAT3 and TrkA signaling pathways have been separately implicated in aggressive breast cancers; however, whether they are co-activated or undergo functional interaction has not been thoroughly investigated. Herein we report, for the first time that STAT3 and TrkA are significantly co-overexpressed and co-activated in triple-negative breast cancer (TNBC) and HER2-enriched breast cancer, as shown by immunohistochemical staining and data mining. Through immunofluorescence staining-confocal microscopy and immunoprecipitation-Western blotting, we found that TrkA and STAT3 co-localize and physically interact in the cytoplasm, and the interaction is dependent on STAT3-Y705 phosphorylation. TrkA-STAT3 interaction leads to STAT3 phosphorylation at Y705 by TrkA in breast cancer cells and cell-free kinase assays, indicating that STAT3 is a novel substrate of TrkA. β-NGF-mediated TrkA activation induces TrkA-STAT3 interaction, STAT3 nuclear transport and transcriptional activity, and the expression of STAT3 target genes,

Indexed as

breast cancercancer stem cellsMYCSOX2STAT3TrkA

Identifiers

PMID34066153
PMCPMC8150921
OpenAlexW3160472898

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.