Evidence map›Paper›PMID 31010006›Full record

ArticleInternational journal of molecular sciences2019

Nonsteroidal Anti-Inflammatory Drugs Prevent Vincristine-Dependent Cancer-Associated Fibroblasts Formation.

Marta Ewelina Wawro, Katarzyna Sobierajska, Wojciech Michał Ciszewski, Jolanta Niewiarowska

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2019. 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
1.2field-weighted citation impact, top 22% 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, 30 citations in OpenAlex.

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  14. Cancer-associated fibroblasts in colorectal cancer.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2022
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  18. The Role of Interleukins in Colorectal Cancer.International journal of biological sciences · 2020
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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

4 authors at 1 institution in 1 country.

Marta Ewelina WawroDepartment of Molecular Cell Mechanisms, Medical University of Lodz, Mazowiecka 6/8, 92-215 Lodz, Poland. marta.wawro@umed.lodz.pl.
Katarzyna SobierajskaDepartment of Molecular Cell Mechanisms, Medical University of Lodz, Mazowiecka 6/8, 92-215 Lodz, Poland. katarzyna.sobierajska@umed.lodz.pl.ORCID 0000-0003-3510-0098
Wojciech Michał CiszewskiDepartment of Molecular Cell Mechanisms, Medical University of Lodz, Mazowiecka 6/8, 92-215 Lodz, Poland. wojciech.ciszewski@umed.lodz.pl.ORCID 0000-0001-6251-6043
Jolanta NiewiarowskaDepartment of Molecular Cell Mechanisms, Medical University of Lodz, Mazowiecka 6/8, 92-215 Lodz, Poland. jolanta.niewiarowska@umed.lodz.pl.ORCID 0000-0003-0561-7766
Medical University of Lodz · PL

Funding

Narodowe Centrum Badań i Rozwoju Pol-Nor/209521/5/2013Narodowe Centrum Nauki 2017/26/D/NZ7/00633Uniwersytet Medyczny w Lodzi 502-03/6-171-02/502-64-120
6 · The paper itself

Abstract

Vincristine is used in the clinical treatment of colon cancer, especially in patients diagnosed in the advanced phase of cancer development. Unfortunately, similar to other agents used during antitumor therapy, vincristine might induce chemoresistance. Studies of this process focus mainly on the analysis of the molecular mechanisms within cancer, usually ignoring the role of stromal cells. Our present findings confirm that vincristine stimulates the secretion of tumor growth factors class beta and interleukin-6 from cancer-associated fibroblasts as a result of paracrine stimulation by cancer cells. Based on alterations in morphology, modulation of capillary formation, and changes in endothelial and mesenchymal marker profile, our findings demonstrate that higher levels of tumor growth factor-βs and interleukin-6 enhance cancer-associated fibroblast-like cell formation through endothelial-mesenchymal transition and that nonsteroidal anti-inflammatory drug treatment (aspirin and ibuprofen) is able to inhibit this phenomenon. The process appears to be regulated by the rate of microtubule polymerization, depending on β-tubulin composition. While higher levels of tubulin-β2 and tubulin-β4 caused slowed polymerization and reduced the level of factors secreted to the extracellular matrix, tubulin-β3 induced the opposite effect. We conclude that nonsteroidal anti-inflammatory drugs should be considered for use during vincristine monotherapy in the treatment of patients diagnosed with colorectal cancer.

Indexed as

Anti-Inflammatory Agents, Non-SteroidalCancer-Associated FibroblastsCell CommunicationCell Line, TumorCell TransdifferentiationColonic NeoplasmsCulture Media, ConditionedCytokinesEndothelial CellsEndotheliumHumansMesodermMicrotubulesPolymerizationTubulinVincristineAnti-Inflammatory Agents, Non-SteroidalCulture Media, ConditionedCytokinesTubulinVincristineaspirinCAFscolon cancerEndMTibuprofenIL-6immunomodulationmicrotubulesTGF-βsvincristine

Identifiers

PMID31010006
PMCPMC6515011
OpenAlexW2935938156

What OpenQuestion holds

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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.