Evidence map›Paper›PMID 26399191›Full record

ArticleScientific reports2015

Opposite Effects of M1 and M2 Macrophage Subtypes on Lung Cancer Progression.

Ang Yuan, Yi-Jing Hsiao, Hsuan-Yu Chen, Huei-Wen Chen, Chao-Chi Ho, Yu-Yun Chen, Yi-Chia Liu, Tsai-Hsia Hong, Sung-Liang Yu, Jeremy J W Chen and 1 more

Abstract read
In one paragraph

Article in Scientific reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 224 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
224citing papers in PubMed, 3 pooled it
–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

224 citing papers in PubMed, 3 syntheses or guidelines pooled it.

  1. Pooled it
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  8. Immunity and Beyond: Emerging Roles of Monocytes and Macrophages in Cancer.Advances in experimental medicine and biology · 2026
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164 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

11 authors.

Ang YuanDepartments of Chest Medicine and Emergency Medicine, National Taiwan University Hospital, Taipei, Taiwan.
Yi-Jing HsiaoDepartment of Clinical Laboratory Sciences and Medical Biotechnology, National Taiwan University College of Medicine, Taipei, Taiwan.
Hsuan-Yu ChenInstitute of Statistical Science, Academia Sinica, Taipei, Taiwan.
Huei-Wen ChenGraduate Institute of Toxicology, National Taiwan University College of Medicine, Taipei, Taiwan.
Chao-Chi HoDepartment of Internal Medicine, National Taiwan University College of Medicine, Taipei, Taiwan.
Yu-Yun ChenGraduate Institute of Toxicology, National Taiwan University College of Medicine, Taipei, Taiwan.
Yi-Chia LiuDepartments of Chest Medicine and Emergency Medicine, National Taiwan University Hospital, Taipei, Taiwan.
Tsai-Hsia HongDepartments of Surgery, National Taiwan University Hospital, Taipei, Taiwan.
Sung-Liang YuDepartment of Clinical Laboratory Sciences and Medical Biotechnology, National Taiwan University College of Medicine, Taipei, Taiwan.
Jeremy J W ChenInstitute of Biomedical Sciences, National Chung-Hsing University, Taichung, Taiwan.
Pan-Chyr YangDepartment of Internal Medicine, National Taiwan University College of Medicine, Taipei, Taiwan.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Macrophages in a tumor microenvironment have been characterized as M1- and M2-polarized subtypes. Here, we discovered the different macrophages' impacts on lung cancer cell A549. The M2a/M2c subtypes promoted A549 invasion and xenograft tumor growth. The M1 subtype suppressed angiogenesis. M1 enhanced the sensitivity of A549 to cisplatin and decreased the tube formation activity and cell viability of A549 cells by inducing apoptosis and senescence. Different macrophage subtypes regulated genes involved in the immune response, cytoskeletal remodeling, coagulation, cell adhesion, and apoptosis pathways in A549 cells, which was a pattern that correlated with the altered behaviors of the A549 cells. Furthermore, we found that the identified M1/M2 gene signatures were significantly correlated with the extended overall survival of lung cancer patients. These results suggest that M1/M2 gene expression signature may be used as a prognostic indicator for lung cancer patients, and M1/M2 polarization may be a target of investigation of immune-modulating therapies for lung cancer in the future.

Indexed as

PhenotypeAnimalsAntineoplastic AgentsBiomarkersCell Line, TumorCell ProliferationCell SurvivalCluster AnalysisDrug Resistance, NeoplasmFemaleGene Expression ProfilingHumansImmunophenotypingKaplan-Meier EstimateLung NeoplasmsMacrophagesAntineoplastic AgentsBiomarkers

Identifiers

PMID26399191
PMCPMC4585843

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Registered trials

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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.