Evidence map›Paper›PMID 30764543›Full record

ArticleInternational journal of molecular sciences2019

Effect of Chemokine (C-C Motif) Ligand 7 (CCL7) and Its Receptor (CCR2) Expression on Colorectal Cancer Behaviors.

Ewa Kurzejamska, Mariusz Sacharczuk, Natalia Landázuri, Oksana Kovtonyuk, Marzena Lazarczyk, Sharan Ananthaseshan, Zbigniew Gaciong, Piotr Religa

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 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.4field-weighted citation impact, top 17% 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

15 citing papers in PubMed, 21 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 2 institutions in 2 countries.

Ewa KurzejamskaDepartment of Medicine, Centre for Molecular Medicine, Karolinska Institute, 171 76 Stockholm, Sweden. ewa.kurzejamska@ki.se.ORCID 0000-0002-8050-6516
Mariusz SacharczukDepartment of Internal Medicine, Hypertension and Vascular Diseases, Medical University of Warsaw, 02 097 Warsaw, Poland. m.sacharczuk@ighz.pl.ORCID 0000-0002-6309-5292
Natalia LandázuriDepartment of Medicine, Centre for Molecular Medicine, Karolinska Institute, 171 76 Stockholm, Sweden. natalia.landazuri@ki.se.
Oksana KovtonyukDepartment of Internal Medicine, Hypertension and Vascular Diseases, Medical University of Warsaw, 02 097 Warsaw, Poland. kseniya_kovtonyuk@yahoo.com.
Marzena LazarczykDepartment of Internal Medicine, Hypertension and Vascular Diseases, Medical University of Warsaw, 02 097 Warsaw, Poland. marzena.lazarczyk@gmail.com.ORCID 0000-0002-1938-8143
Sharan AnanthaseshanDepartment of Medicine, Centre for Molecular Medicine, Karolinska Institute, 171 76 Stockholm, Sweden. sharan.anand23@gmail.com.
Zbigniew GaciongDepartment of Internal Medicine, Hypertension and Vascular Diseases, Medical University of Warsaw, 02 097 Warsaw, Poland. zbigniew.gaciong@wum.edu.pl.
Piotr ReligaDepartment of Medicine, Centre for Molecular Medicine, Karolinska Institute, 171 76 Stockholm, Sweden. piotr.religa@ki.se.
Medical University of Warsaw · PLKarolinska Institutet · SE

Funding

Fundacja na rzecz Nauki Polskiej -Karolinska Institutet -Narodowe Centrum Nauki 2014/15/B/NZ5/03566Narodowe Centrum Nauki DEC-2013/11/N/NZ4/02288Robert Lundbergs Minnesstiftelse -Seventh Framework Programme -
6 · The paper itself

Abstract

Colorectal cancer is the source of one of the most common cancer-related deaths worldwide, where the main cause of patient mortality remains metastasis. The aim of this study was to determine the role of CCL7 (chemokine (C-C motif) ligand 7) in tumor progression and finding whether it could predict survival of colorectal cancer patients. Initially, our study focused on the crosstalk between mesenchymal stem cells (MSCs) and CT26 colon carcinoma cells and resulted in identifying CCL7 as a chemokine upregulated in CT26 colon cancer cells cocultured with MSCs, compared with CT26 in monoculture in vitro. Moreover, we showed that MSCs enhance CT26 tumor cell proliferation and migration. We analyzed the effect of CCL7 overexpression on tumor progression in a murine CT26 model, where cells overexpressing CCL7 accelerated the early phase of tumor growth and caused higher lung metastasis rates compared with control mice. Microarray analysis revealed that tumors overexpressing CCL7 had lower expression of immunoglobulins produced by B lymphocytes. Additionally, using Jh mutant mice, we confirmed that in the CT26 model, CCL7 has an immunoglobulin-, and thereby, B-cell-dependent effect on metastasis formation. Finally, higher expression of CCL7 receptor CCR2 (C-C chemokine receptor type 2) was associated with shorter overall survival of colorectal cancer patients. Altogether, we showed that CCL7 is essentially involved in the progression of colorectal cancer in a CT26 mouse model and that the expression of its receptor CCR2 could be related to a different outcome pattern of patients with colorectal carcinoma.

Indexed as

Gene Expression Regulation, NeoplasticUp-RegulationAgedAged, 80 and overAnimalsCell Line, TumorCell MovementCell ProliferationChemokine CCL7Colonic NeoplasmsDisease ProgressionFemaleHumansMaleMiceMice, Inbred BALB CChemokine CCL7Receptors, CCR2CCL7chemokinecolon cancerimmunoglobulinsmetastasistumor growth

Identifiers

PMID30764543
PMCPMC6387027
OpenAlexW2914330597

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.