Evidence map›Paper›PMID 31801938›Full record

ArticleCell death & disease2019

Gastric cancer-derived mesenchymal stromal cells trigger M2 macrophage polarization that promotes metastasis and EMT in gastric cancer.

Wei Li, Xu Zhang, Fenglei Wu, Ying Zhou, Zengtao Bao, Haining Li, Ping Zheng, Shaolin Zhao

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 225 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
225citing papers in PubMed, 2 pooled it
15.7field-weighted citation impact, top 1% 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

225 citing papers in PubMed, 2 syntheses or guidelines pooled it, 377 citations in OpenAlex.

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165 more citing papers are in PubMed but not listed here.

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 3 institutions in 1 country.

Wei LiCenter of Research Laboratory, The First People's Hospital of Lianyungang, Lianyungang, 222001, China. medical112@126.com.
Xu ZhangJiangsu Key Laboratory of Medical Science and Laboratory Medicine, Jiangsu University, Zhenjiang, 212013, China.
Fenglei WuDepartment of Oncology, The First People's Hospital of Lianyungang, Lianyungang, 222001, China.
Ying ZhouCenter of Research Laboratory, The First People's Hospital of Lianyungang, Lianyungang, 222001, China.
Zengtao BaoDepartment of Gastrointestinal Surgery, The First People's Hospital of Lianyungang, Lianyungang, 222001, China.
Haining LiCenter of Research Laboratory, The First People's Hospital of Lianyungang, Lianyungang, 222001, China.
Ping ZhengCenter of Research Laboratory, The First People's Hospital of Lianyungang, Lianyungang, 222001, China.
Shaolin ZhaoCenter of Research Laboratory, The First People's Hospital of Lianyungang, Lianyungang, 222001, China. zhaoshaolin1@163.com.
The First People’s Hospital of Lianyungang · CNJiangsu University · CNNanjing Medical University · CN

Funding

Jiangsu Postdoctoral Research Foundation (Jiangsu Province Postdoctoral Research Foundation) 1501079ANational Natural Science Foundation of China (National Science Foundation of China) 81402280National Natural Science Foundation of China (National Science Foundation of China) 81672416Natural Science Foundation of Jiangsu Province (Jiangsu Provincial Natural Science Foundation) BK20161296
6 · The paper itself

Abstract

Resident macrophages in the tumor microenvironment exert a dual role in tumor progression. So far, the mechanism of intratumoral macrophage generation is still largely unknown. In the present study, the importance of macrophages in the pro-tumor role of gastric cancer-derived mesenchymal stromal cells (GC-MSCs) was observed in a mouse xenograft model with macrophage depletion. In gastric cancer tissues, high expression levels of Ym-1, Fizz-1, arginase-1, and CCR-2, as well as a low expression level of iNOS, were verified, and co-localization of GC-MSCs and tumor-associated macrophages (TAMs) was observed by dual immunofluorescence histochemistry. TAMs isolated from gastric cancer tissues predominantly displayed an M2 phenotype. In a co-culture system, the contribution of GC-MSCs to M2 polarization of macrophages was confirmed by the M2-related protein expression, M2-like immunophenotype and cytokine profile of GC-MSC-primed macrophages in vitro. Blockade of IL-6/IL-8 by neutralizing antibodies significantly attenuated the promoting effect of GC-MSCs on M2-like macrophage polarization via the JAK2/STAT3 signaling pathway. In addition, GC-MSC-primed macrophages promoted the migration and invasion of gastric cancer cells, and the process of EMT in gastric cancer cells was significantly enhanced by GC-MSC-primed macrophage treatment. Our study showed that tumor-promoting GC-MSCs contribute to M2 macrophage polarization within the gastric cancer niche through considerable secretion of IL-6 and IL-8. These GC-MSC-primed macrophages can subsequently prompt gastric cancer metastasis via EMT promotion in gastric cancer cells.

Indexed as

AnimalsArginaseCell Line, TumorCell MovementCell PolarityCell ProliferationEpithelial-Mesenchymal TransitionGene Expression Regulation, NeoplasticHeterograftsHumansInterleukin-6Interleukin-8Macrophage ActivationMacrophagesMesenchymal Stem CellsMiceARG1 protein, humanArginaseCCR2 protein, humanInterleukin-6Interleukin-8Receptors, CCR2

Identifiers

PMID31801938
PMCPMC6892854
OpenAlexW2992471949

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.