Evidence map›Paper›PMID 29968778›Full record

ArticleScientific reports2018

Pirfenidone decreases mesothelioma cell proliferation and migration via inhibition of ERK and AKT and regulates mesothelioma tumor microenvironment in vivo.

Chang Li, Veronika Rezov, Emmi Joensuu, Ville Vartiainen, Mikko Rönty, Miao Yin, Marjukka Myllärniemi, Katri Koli

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
5.1field-weighted citation impact, top 4% 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

29 citing papers in PubMed, 46 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

8 authors at 1 institution in 3 countries.

Chang LiResearch Programs Unit, Translational Cancer Biology, University of Helsinki, Helsinki, Finland.
Veronika RezovResearch Programs Unit, Translational Cancer Biology, University of Helsinki, Helsinki, Finland.
Emmi JoensuuResearch Programs Unit, Translational Cancer Biology, University of Helsinki, Helsinki, Finland.
Ville VartiainenResearch Programs Unit, Translational Cancer Biology, University of Helsinki, Helsinki, Finland.ORCID 0000-0002-9833-6965
Mikko RöntyDepartment of Pathology, University of Helsinki and Fimlab laboratories, Pathology, Tampere, Finland.
Miao YinResearch Programs Unit, Translational Cancer Biology, University of Helsinki, Helsinki, Finland.
Marjukka MyllärniemiUniversity of Helsinki and Helsinki University Hospital, Heart and Lung Center and HUH diagnostics, Pulmonary Medicine, Helsinki, Finland.
Katri KoliResearch Programs Unit, Translational Cancer Biology, University of Helsinki, Helsinki, Finland. katri.koli@helsinki.fi.
University of Helsinki · FI

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Malignant mesothelioma is an aggressive cancer with poor prognosis. It is characterized by prominent extracellular matrix, mesenchymal tumor cell phenotypes and chemoresistance. In this study, the ability of pirfenidone to alter mesothelioma cell proliferation and migration as well as mesothelioma tumor microenvironment was evaluated. Pirfenidone is an anti-fibrotic drug used in the treatment of idiopathic pulmonary fibrosis and has also anti-proliferative activities. Mesothelioma cell proliferation was decreased by pirfenidone alone or in combination with cisplatin. Pirfenidone also decreased significantly Transwell migration/invasion and 3D collagen invasion. This was associated with increased BMP pathway activity, decreased GREM1 expression and downregulation of MAPK/ERK and AKT/mTOR signaling. The canonical Smad-mediated TGF-β signaling was not affected by pirfenidone. However, pirfenidone blocked TGF-β induced upregulation of ERK and AKT pathways. Treatment of mice harboring mesothelioma xenografts with pirfenidone alone did not reduce tumor proliferation in vivo. However, pirfenidone modified the tumor microenvironment by reducing the expression of extracellular matrix associated genes. In addition, GREM1 expression was downregulated by pirfenidone in vivo. By reducing two major upregulated pathways in mesothelioma and by targeting tumor cells and the microenvironment pirfenidone may present a novel anti-fibrotic and anti-cancer adjuvant therapy for mesothelioma.

Indexed as

AnimalsCell Line, TumorCell MovementCell ProliferationCollagenExtracellular MatrixFemaleFibroblastsFibrosisHumansLung NeoplasmsMAP Kinase Signaling SystemMesotheliomaMesothelioma, MalignantMiceMice, Inbred BALB CCollagenpirfenidoneProto-Oncogene Proteins c-aktPyridones

Identifiers

PMID29968778
PMCPMC6030186
OpenAlexW2810553723

What Socratic 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 Socratic graph.