Evidence map›Paper›PMID 30190333›Full record

ArticleEMBO molecular medicine2018

Stress signaling in breast cancer cells induces matrix components that promote chemoresistant metastasis.

Jacob Insua-Rodríguez, Maren Pein, Tsunaki Hongu, Jasmin Meier, Arnaud Descot, Camille M Lowy, Etienne De Braekeleer, Hans-Peter Sinn, Saskia Spaich, Marc Sütterlin and 2 more

Open access · goldAbstract read
In one paragraph

Article in EMBO molecular medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers.

0numbers the graph read from it
0cells of the map it votes in
61citing papers in PubMed
6.1field-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

61 citing papers in PubMed, 121 citations in OpenAlex.

  1. Trial
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  8. Resveratrol-rich extract fromCytotechnology · 2025
    Article
  9. Dynamics of inflammatory signals within the tumor microenvironment.World journal of experimental medicine · 2025
    Review
  10. Article
  11. Article
  12. Article
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  15. Exploring the multifaceted role of obesity in breast cancer progression.Frontiers in cell and developmental biology · 2024
    Review
  16. Article
  17. Article
  18. Article
  19. Review
  20. Article

1 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

12 authors at 3 institutions in 2 countries.

Jacob Insua-RodríguezHeidelberg Institute for Stem Cell Technology and Experimental Medicine (HI-STEM gGmbH), Heidelberg, Germany.
Maren PeinHeidelberg Institute for Stem Cell Technology and Experimental Medicine (HI-STEM gGmbH), Heidelberg, Germany.
Tsunaki HonguHeidelberg Institute for Stem Cell Technology and Experimental Medicine (HI-STEM gGmbH), Heidelberg, Germany.
Jasmin MeierHeidelberg Institute for Stem Cell Technology and Experimental Medicine (HI-STEM gGmbH), Heidelberg, Germany.
Arnaud DescotHeidelberg Institute for Stem Cell Technology and Experimental Medicine (HI-STEM gGmbH), Heidelberg, Germany.
Camille M LowyHeidelberg Institute for Stem Cell Technology and Experimental Medicine (HI-STEM gGmbH), Heidelberg, Germany.
Etienne De BraekeleerHeidelberg Institute for Stem Cell Technology and Experimental Medicine (HI-STEM gGmbH), Heidelberg, Germany.
Hans-Peter SinnInstitute of Pathology, University of Heidelberg, Heidelberg, Germany.
Saskia SpaichDepartment of Obstetrics and Gynecology, University Medical Centre Mannheim, Heidelberg University, Mannheim, Germany.
Marc SütterlinDepartment of Obstetrics and Gynecology, University Medical Centre Mannheim, Heidelberg University, Mannheim, Germany.
Andreas SchneeweissNational Center for Tumor Diseases-NCT, Heidelberg, Germany.
Thordur OskarssonHeidelberg Institute for Stem Cell Technology and Experimental Medicine (HI-STEM gGmbH), Heidelberg, Germany t.oskarsson@dkfz.de.ORCID 0000-0002-0983-6969
German Cancer Research Center · DEHeidelberg University · DEUniversity of Tsukuba · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Metastatic progression remains a major burden for cancer patients and is associated with eventual resistance to prevailing therapies such as chemotherapy. Here, we reveal how chemotherapy induces an extracellular matrix (ECM), wound healing, and stem cell network in cancer cells via the c-Jun N-terminal kinase (JNK) pathway, leading to reduced therapeutic efficacy. We find that elevated JNK activity in cancer cells is linked to poor clinical outcome in breast cancer patients and is critical for tumor initiation and metastasis in xenograft mouse models of breast cancer. We show that JNK signaling enhances expression of the ECM and stem cell niche components osteopontin, also called secreted phosphoprotein 1 (SPP1), and tenascin C (TNC), that promote lung metastasis. We demonstrate that both

Indexed as

Drug Resistance, NeoplasmSignal TransductionAnimalsBreast NeoplasmsCell MovementCell ProliferationDisease Models, AnimalExtracellular MatrixFemaleHeterograftsHumansJNK Mitogen-Activated Protein KinasesMiceNeoplasm MetastasisNeoplasm TransplantationNeoplastic Stem CellsJNK Mitogen-Activated Protein Kinasesbreast cancer metastasischemotherapy resistanceextracellular matrixstem cell nichestress

Identifiers

PMID30190333
PMCPMC6180299
OpenAlexW2891029625

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.