Evidence map›Paper›PMID 26000098›Full record

ArticleGenes & cancer2015

Granulin, a novel STAT3-interacting protein, enhances STAT3 transcriptional function and correlates with poorer prognosis in breast cancer.

Jennifer E Yeh, Simion Kreimer, Sarah R Walker, Megan M Emori, Hannah Krystal, Andrea Richardson, Alexander R Ivanov, David A Frank

Open access · diamondAbstract read
In one paragraph

Article in Genes & cancer, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.3field-weighted citation impact, top 18% 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

17 citing papers in PubMed, 25 citations in OpenAlex.

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  12. STAT3 Interactors as Potential Therapeutic Targets for Cancer Treatment.International journal of molecular sciences · 2018
    Review
  13. Article
  14. Article
  15. Over-Expression of POU Class 1 Homeobox 1 Transcription Factor (Pit-1) Predicts Poor Prognosis for Breast Cancer Patients.Medical science monitor : international medical journal of experimental and clinical research · 2016
    Article
  16. 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

8 authors at 4 institutions in 1 country.

Jennifer E YehDepartment of Medical Oncology, Dana-Farber Cancer Institute, Boston, MA.
Simion KreimerBarnett Institute of Chemical and Biological Analysis, Northeastern University, Boston, MA.
Sarah R WalkerDepartment of Medical Oncology, Dana-Farber Cancer Institute, Boston, MA ; Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA.
Megan M EmoriDepartment of Medical Oncology, Dana-Farber Cancer Institute, Boston, MA.
Hannah KrystalDepartment of Medical Oncology, Dana-Farber Cancer Institute, Boston, MA.
Andrea RichardsonDepartment of Pathology, Brigham and Women's Hospital and Harvard Medical School, Boston, MA.
Alexander R IvanovBarnett Institute of Chemical and Biological Analysis, Northeastern University, Boston, MA.
David A FrankDepartment of Medical Oncology, Dana-Farber Cancer Institute, Boston, MA ; Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA.
Dana-Farber Cancer Institute · USHarvard University · USNortheastern University · USBrigham and Women's Hospital · US

Funding

Molecular, Cellular, & Developmental Dynamics PhD ProgramT32GM007226 · NIGMS · HARVARD UNIVERSITY (MEDICAL SCHOOL) · PI VAN VACTOR, DAVID L. · 1985 to 2021
$14.4M
Dual STAT3/NF-kB Inhibitors for Targeted Cancer TherapyR01CA160979 · NCI · DANA-FARBER CANCER INST · PI FRANK, DAVID A. · 2012 to 2016
$1.8M
Defining the CD44-STAT3 axis in the pathogenesis of triple-negative breast cancerF30CA180340 · NCI · HARVARD MEDICAL SCHOOL · PI YEH, JENNIFER ELYNN · 2013 to 2016
$162k
NCI NIH HHS F30 CA180340NCI NIH HHS R01 CA160979NIGMS NIH HHS T32 GM007226
6 · The paper itself

Abstract

Since the neoplastic phenotype of a cell is largely driven by aberrant gene expression patterns, increasing attention has been focused on transcription factors that regulate critical mediators of tumorigenesis such as signal transducer and activator of transcription 3 (STAT3). As proteins that interact with STAT3 may be key in addressing how STAT3 contributes to cancer pathogenesis, we took a proteomics approach to identify novel STAT3-interacting proteins. We performed mass spectrometry-based profiling of STAT3-containing complexes from breast cancer cells that have constitutively active STAT3 and are dependent on STAT3 function for survival. We identified granulin (GRN) as a novel STAT3-interacting protein that was necessary for both constitutive and maximal leukemia inhibitory factor (LIF)induced STAT3 transcriptional activity. GRN enhanced STAT3 DNA binding and also increased the time-integrated amount of LIF-induced STAT3 activation in breast cancer cells. Furthermore, silencing GRN neutralized STAT3-mediated tumorigenic phenotypes including viability, clonogenesis, and migratory capacity. In primary breast cancer samples, GRN mRNA levels were positively correlated with STAT3 gene expression signatures and with reduced patient survival. These studies identify GRN as a functionally important STAT3-interacting protein that may serve as an important prognostic biomarker and potential therapeutic target in breast cancer.

Indexed as

breast cancerinteracting proteinSTAT3

Identifiers

PMID26000098
PMCPMC4426952
OpenAlexW2108610676

What OpenQuestion holds

Textmetadata
LicenceCC BY
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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.