Evidence map›Paper›PMID 26284488›Full record

ArticleOncotarget2015

Colorectal cancer-promoting activity of the senescent peritoneal mesothelium.

Justyna Mikuła-Pietrasik, Patrycja Sosińska, Konstantin Maksin, Mał Gorzata Kucińska, Hanna Piotrowska, Marek Murias, Aldona Woźniak, Dariusz Szpurek, Krzysztof Książek

Open access · diamondAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
2.8field-weighted citation impact, top 9% 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

28 citing papers in PubMed, 43 citations in OpenAlex.

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  8. Extracellular RNA in melanoma: Advances, challenges, and opportunities.Frontiers in cell and developmental biology · 2023
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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

9 authors at 1 institution in 1 country.

Justyna Mikuła-PietrasikDepartment of Pathophysiology, Poznań„ University of Medical Sciences, Poznań„, Poland.
Patrycja SosińskaDepartment of Pathophysiology, Poznań„ University of Medical Sciences, Poznań„, Poland.
Konstantin MaksinDepartment of Clinical Pathology, Poznań„ University of Medical Sciences, PoznaÅń, Poland.
Mał Gorzata KucińskaDepartment of Toxicology, Poznań„ University of Medical Sciences, Poznań„, Poland.
Hanna PiotrowskaDepartment of Toxicology, Poznań„ University of Medical Sciences, Poznań„, Poland.
Marek MuriasDepartment of Toxicology, Poznań„ University of Medical Sciences, Poznań„, Poland.
Aldona WoźniakDepartment of Clinical Pathology, Poznań„ University of Medical Sciences, PoznaÅń, Poland.
Dariusz SzpurekDivision of Gynecological Surgery, Poznań„ University of Medical Sciences, Poznań„, Poland.
Krzysztof KsiążekDepartment of Pathophysiology, Poznań„ University of Medical Sciences, Poznań„, Poland.
Poznan University of Medical Sciences · PL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Gastrointestinal cancers metastasize into the peritoneal cavity in a process controlled by peritoneal mesothelial cells (HPMCs). In this paper we examined if senescent HPMCs can intensify the progression of colorectal (SW480) and pancreatic (PSN-1) cancers in vitro and in vivo. Experiments showed that senescent HPMCs stimulate proliferation, migration and invasion of SW480 cells, and migration of PSN-1 cells. When SW480 cells were injected i.p. with senescent HPMCs, the dynamics of tumor formation and vascularization were increased. When xenografts were generated using PSN-1 cells, senescent HPMCs failed to favor their growth. SW480 cells subjected to senescent HPMCs displayed up-regulated expression of transcripts for various pro-cancerogenic agents as well as increased secretion of their products. Moreover, they underwent an epithelial-mesenchymal transition in the Smad 2/3-Snail1-related pathway. The search for mediators of senescent HPMC activity showed that increased SW480 cell proliferation was stimulated by IL-6, migration by CXCL8 and CCL2, invasion by IL-6, MMP-3 and uPA, and epithelial-mesenchymal transition by TGF-β1. Secretion of these agents by senescent HPMCs was increased in an NF-κB- and p38 MAPK-dependent mechanism. Collectively, our findings indicate that in the peritoneum senescent HPMCs may create a metastatic niche in which critical aspects of cancer progression become intensified.

Indexed as

Cellular SenescenceParacrine CommunicationAnimalsCell Line, TumorCell MovementCell ProliferationColorectal NeoplasmsEpithelial-Mesenchymal TransitionGene Expression Regulation, NeoplasticHumansMice, SCIDNeoplasm InvasivenessPancreatic NeoplasmsPeritoneal NeoplasmsPeritoneumSignal Transductioncellular senescencegastrointestinal cancersmesothelial cellsmice xenograftsperitoneal cavity

Identifiers

PMID26284488
PMCPMC4745719
OpenAlexW2179650400

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.