Evidence map›Paper›PMID 31086083›Full record

ArticleCancers2019

A Unique Pattern of Mesothelial-Mesenchymal Transition Induced in the Normal Peritoneal Mesothelium by High-Grade Serous Ovarian Cancer.

Martyna Pakuła, Paweł Uruski, Arkadiusz Niklas, Aldona Woźniak, Dariusz Szpurek, Andrzej Tykarski, Justyna Mikuła-Pietrasik, Krzysztof Książek

Abstract read
In one paragraph

Article in Cancers, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
–field-weighted citation impact
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

10 citing papers in PubMed.

  1. Article
  2. Review
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  8. Article
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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.

Martyna PakułaDepartment of Hypertensiology, Angiology and Internal Medicine, Poznan University of Medical Sciences, Długa 1/2 Str., 61-848 Poznan, Poland. mpakula@ump.edu.pl.
Paweł UruskiDepartment of Hypertensiology, Angiology and Internal Medicine, Poznan University of Medical Sciences, Długa 1/2 Str., 61-848 Poznan, Poland. puruski@ump.edu.pl.
Arkadiusz NiklasDepartment of Hypertensiology, Angiology and Internal Medicine, Poznan University of Medical Sciences, Długa 1/2 Str., 61-848 Poznan, Poland. aniklas@mp.pl.
Aldona WoźniakDepartment of Clinical Pathology, Poznan University of Medical Sciences, Przybyszewskiego 49 Str., 60-355 Poznan, Poland. aldona.wozniak@wp.pl.
Dariusz SzpurekDivision of Gynecological Surgery, Poznan University of Medical Sciences, Polna 33 Str, 60-535 Poznan, Poland. dszpurek@gmail.com.
Andrzej TykarskiDepartment of Hypertensiology, Angiology and Internal Medicine, Poznan University of Medical Sciences, Długa 1/2 Str., 61-848 Poznan, Poland. tykarski@o2.pl.
Justyna Mikuła-PietrasikDepartment of Hypertensiology, Angiology and Internal Medicine, Poznan University of Medical Sciences, Długa 1/2 Str., 61-848 Poznan, Poland. jmikula@ump.edu.pl.
Krzysztof KsiążekDepartment of Hypertensiology, Angiology and Internal Medicine, Poznan University of Medical Sciences, Długa 1/2 Str., 61-848 Poznan, Poland. kksiazek@ump.edu.pl.

Funding

Narodowe Centrum Nauki 2014/15/B/NZ3/00421Narodowe Centrum Nauki 2017/25/B/NZ3/00122
6 · The paper itself

Abstract

The study was designed to establish whether high aggressiveness of high-grade serous ovarian cancer cells (HGSOCs), which display rapid growth, advanced stage at diagnosis and the highest mortality among all epithelial ovarian cancer histotypes, may be linked with a specific pattern of mesothelial-mesenchymal transition (MMT) elicited by these cells in normal peritoneal mesothelial cells (PMCs). Experiments were performed on primary PMCs, stable and primary ovarian cancer cells, tumors from patients with ovarian cancer, and laboratory animals. Results of in vitro and in vivo tests showed that MMT triggered by HGSOCs (primary cells and OVCAR-3 line) is far more pronounced than the process evoked by cells representing less aggressive ovarian cancer histotypes (A2780, SKOV-3). Mechanistically, HGSOCs induce MMT via Smad 2/3, ILK, TGF-1, HGF, and IGF-1, whereas A2780 and SKOV-3 cells via exclusively Smad 2/3 and HGF. The conditioned medium from PMCs undergoing MMT promoted the progression of cancer cells and the effects exerted by the cells triggered to undergo MMT by the HGSOCs were significantly stronger than those related to the activity of their less aggressive counterparts. Our findings indicate that MMT in PMCs provoked by HGSOCs is stronger, proceeds via different mechanisms and has more procancerous characteristics than MMT provoked by less aggressive cancer histotypes, which may at least partly explain high aggressiveness of HGSOCs.

Indexed as

cancer metastasesmesothelial cellsmesothelial-mesenchymal transitionovarian cancerperitoneal cavity

Identifiers

PMID31086083
PMCPMC6562987

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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.