Evidence map›Paper›PMID 27259262›Full record

ArticleOncotarget2016

MLLT11/AF1q boosts oncogenic STAT3 activity through Src-PDGFR tyrosine kinase signaling.

Jino Park, Soojin Kim, Joongho Joh, Scot C Remick, Donald M Miller, Jun Yan, Zeyad Kanaan, Ju-Hsien Chao, Maxwell M Krem, Soumit K Basu and 5 more

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
3.2field-weighted citation impact, top 7% 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

20 citing papers in PubMed, 31 citations in OpenAlex.

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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

15 authors at 5 institutions in 3 countries.

Jino ParkJames Graham Brown Cancer Center, University of Louisville School of Medicine, Louisville, KY, USA.
Soojin KimJames Graham Brown Cancer Center, University of Louisville School of Medicine, Louisville, KY, USA.
Joongho JohJames Graham Brown Cancer Center, University of Louisville School of Medicine, Louisville, KY, USA.
Scot C RemickMaine Medical Center Research Institute, Portland, ME, USA.
Donald M MillerJames Graham Brown Cancer Center, University of Louisville School of Medicine, Louisville, KY, USA.
Jun YanJames Graham Brown Cancer Center, University of Louisville School of Medicine, Louisville, KY, USA.
Zeyad KanaanJames Graham Brown Cancer Center, University of Louisville School of Medicine, Louisville, KY, USA.
Ju-Hsien ChaoJames Graham Brown Cancer Center, University of Louisville School of Medicine, Louisville, KY, USA.
Maxwell M KremJames Graham Brown Cancer Center, University of Louisville School of Medicine, Louisville, KY, USA.
Soumit K BasuJames Graham Brown Cancer Center, University of Louisville School of Medicine, Louisville, KY, USA.
Shotaro HagiwaraDivision of Hematology, Internal Medicine, National Center for Global Health and Medicine, Shinjuku, Japan.
Lukas KennerLudwig Boltzmann Institute for Cancer Research, Vienna, Austria.
Richard MorigglLudwig Boltzmann Institute for Cancer Research, Vienna, Austria.
Kevin D BuntingAflac Cancer and Blood Disorders Center of Children's Healthcare of Atlanta and Emory University School of Medicine, Atlanta, GA, USA.
William TseJames Graham Brown Cancer Center, University of Louisville School of Medicine, Louisville, KY, USA.
University of Louisville · USLudwig Boltzmann Institute for Cancer Research · ATChildren's Healthcare of Atlanta · USMaine Medical Center · USNational Center for Global Health and Medicine · JP

Funding

STAT5 Structure-Function in HematopoiesisR01DK059380 · NIDDK · EMORY UNIVERSITY · PI BUNTING, KEVIN D · 2002 to 2017
$4.2M
NIDDK NIH HHS R01 DK059380
6 · The paper itself

Abstract

Constitutive STAT3 activation by tyrosine phosphorylation of mutated or amplified tyrosine kinases (pYSTAT3) is critical for cancer initiation, progression, invasion, and motility of carcinoma cells. We showed that AF1q is associated with STAT3 signaling in breast cancer cells. In xenograft models, enhanced AF1q expression activated STAT3 and promoted tumor growth and metastasis in immunodeficient NSG mice. The cytokine secretory phenotype of MDA-MB-231LN breast cancer cells with altered AF1q expression revealed changes in expression of platelet-derived growth factor subunit B (PDGF-B). AF1q-induced PDGF-B stimulated motility, migration, and invasion of MDA-MB-231LN cells, and AF1q up-regulated platelet-derived growth factor receptor (PDGFR) signaling. Further, AF1q-induced PDGFR signaling enhanced STAT3 activity through Src kinase activation, which could be blocked by the Src kinase inhibitor PP1. Moreover, AF1q up-regulated tyrosine kinase signaling through PDGFR signaling, which was blockable by imatinib. In conclusion, we demonstrated that enhanced AF1q expression contributes to persistent and oncogenic pYSTAT3 levels in invasive carcinoma cells by activating Src kinase through activation of the PDGF-B/PDGFR cascade. Therefore, AF1q plays an essential role as a cofactor in PDGF-B-driven STAT3 signaling.

Indexed as

AnimalsBreast NeoplasmsCell LineCell Line, TumorCell MovementFemaleHumansMice, Inbred NODMice, KnockoutMice, SCIDNeoplasm InvasivenessNeoplasm ProteinsProto-Oncogene ProteinsReceptors, Platelet-Derived Growth FactorRNAi TherapeuticsSignal TransductionMLLT11 protein, humanNeoplasm ProteinsPDGF receptor tyrosine kinaseProto-Oncogene ProteinsReceptors, Platelet-Derived Growth Factorsrc-Family KinasesSTAT3 Transcription FactorAF1qPDGFPDGFRSrcSTAT3

Identifiers

PMID27259262
PMCPMC5190071
OpenAlexW2409050692

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.