Evidence map›Paper›PMID 29084208›Full record

ArticleOncogene2018

Transcription factor c-Myb inhibits breast cancer lung metastasis by suppression of tumor cell seeding.

L Knopfová, E Biglieri, N Volodko, M Masařík, M Hermanová, J F Glaus Garzón, M Dúcka, T Kučírková, K Souček, J Šmarda and 2 more

Open access · greenAbstract read
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 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
0.6field-weighted citation impact, top 35% 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, 25 citations in OpenAlex.

  1. MAD1L1 and MAD2L1 genes variants in spontaneous miscarriage with aneuploidy.Chromosome research : an international journal on the molecular, supramolecular and evolutionary aspects of chromosome biology · 2026
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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

12 authors at 3 institutions in 3 countries.

L KnopfováDepartment of Experimental Biology, Faculty of Science, Masaryk University, Brno, Czech Republic.
E BiglieriInstitute of Physiology, University of Zurich and Zurich Center for Integrative Human Physiology, Zurich, Switzerland.
N VolodkoDanylo Galytsky Lviv National Medical University, Department of Oncology and Medical Radiology, Lviv, Ukraine.
M MasaříkDepartment of Physiology and Department of Pathological Physiology, Faculty of Medicine, Masaryk University, Brno, Czech Republic.
M HermanováFirst Department of Pathological Anatomy, St. Anne's University Hospital and Faculty of Medicine, Masaryk University, Brno, Czech Republic.
J F Glaus GarzónInstitute of Physiology, University of Zurich and Zurich Center for Integrative Human Physiology, Zurich, Switzerland.
M DúckaDepartment of Experimental Biology, Faculty of Science, Masaryk University, Brno, Czech Republic.
T KučírkováDepartment of Experimental Biology, Faculty of Science, Masaryk University, Brno, Czech Republic.
K SoučekDepartment of Experimental Biology, Faculty of Science, Masaryk University, Brno, Czech Republic.
J ŠmardaDepartment of Experimental Biology, Faculty of Science, Masaryk University, Brno, Czech Republic.
P BenešDepartment of Experimental Biology, Faculty of Science, Masaryk University, Brno, Czech Republic.
L BorsigInstitute of Physiology, University of Zurich and Zurich Center for Integrative Human Physiology, Zurich, Switzerland.ORCID 0000-0003-2263-9545
Masaryk University · CZUniversity of Zurich · CHDanylo Halytsky Lviv National Medical University · UA

Funding

Swiss National Science Foundation 152361Swiss National Science Foundation 152901
6 · The paper itself

Abstract

Metastasis accounts for most of cancer-related deaths. Paracrine signaling between tumor cells and the stroma induces changes in the tumor microenvironment required for metastasis. Transcription factor c-Myb was associated with breast cancer (BC) progression but its role in metastasis remains unclear. Here we show that increased c-Myb expression in BC cells inhibits spontaneous lung metastasis through impaired tumor cell extravasation. On contrary, BC cells with increased lung metastatic capacity exhibited low c-Myb levels. We identified a specific inflammatory signature, including Ccl2 chemokine, that was expressed in lung metastatic cells but was suppressed in tumor cells with higher c-Myb levels. Tumor cell-derived Ccl2 expression facilitated lung metastasis and rescued trans-endothelial migration of c-Myb overexpressing cells. Clinical data show that the identified inflammatory signature, together with a MYB expression, predicts lung metastasis relapse in BC patients. These results demonstrate that the c-Myb-regulated transcriptional program in BCs results in a blunted inflammatory response and consequently suppresses lung metastasis.

Indexed as

Gene Expression Regulation, NeoplasticAnimalsApoptosisBiomarkers, TumorBreast NeoplasmsCell ProliferationChemokine CCL2FemaleHumansLung NeoplasmsMiceMice, Inbred BALB CMice, Inbred C57BLMice, Inbred NODMice, SCIDNeoplasm Recurrence, LocalBiomarkers, TumorCCL2 protein, humanChemokine CCL2Proto-Oncogene Proteins c-myb

Identifiers

PMID29084208
PMCPMC6711763
OpenAlexW2765210128

What OpenQuestion holds

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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.