Evidence map›Paper›PMID 31097690›Full record

ArticleCell death & disease2019

M2 macrophages promote NSCLC metastasis by upregulating CRYAB.

Zhe Guo, Jing Song, Junxia Hao, Hui Zhao, Xiaohui Du, Encheng Li, Yanbin Kuang, Fuquan Yang, Wei Wang, Jiong Deng and 1 more

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 74 papers.

0numbers the graph read from it
0cells of the map it votes in
74citing papers in PubMed
5.4field-weighted citation impact, top 3% 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

74 citing papers in PubMed, 149 citations in OpenAlex.

  1. Review
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  13. Effects of Vinorelbine on M2 Macrophages in Non-Small Cell Lung Cancer.International journal of molecular sciences · 2025
    Article
  14. Review
  15. Article
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  19. Targeted Cancer Therapy-on-A-Chip.Advanced healthcare materials · 2024
    Review
  20. Review

14 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 at 4 institutions in 1 country.

Zhe GuoDepartment of Respiratory Medicine, The Second Hospital, Dalian Medical University, Dalian, China.
Jing SongDepartment of Respiratory Medicine, The Second Hospital, Dalian Medical University, Dalian, China.
Junxia HaoDepartment of Respiratory Medicine, The Second Hospital, Dalian Medical University, Dalian, China.
Hui ZhaoDepartment of Physical Examination Center, The Second Hospital, Dalian Medical University, Dalian, China.
Xiaohui DuDepartment of Scientific Research Center, The Second Hospital, Dalian Medical University, Dalian, China.
Encheng LiDepartment of Respiratory Medicine, The Second Hospital, Dalian Medical University, Dalian, China.
Yanbin KuangDepartment of Respiratory Medicine, The Second Hospital, Dalian Medical University, Dalian, China.ORCID http://orcid.org/0000-0003-3041-7854
Fuquan YangLaboratory of Protein and Peptide Pharmaceuticals and Laboratory of Proteomics, Institute of Biophysics, Chinese Academy of Sciences, Beijing, China.
Wei WangInstitute of Microelectronics, Peking University, Beijing, China. w.wang@pku.edu.cn.
Jiong DengTranslation Medicine Center, Shanghai Chest Hospital, Shanghai Jiao Tong University, Shanghai, China. jiongdeng@shsmu.edu.cn.
Qi WangDepartment of Respiratory Medicine, The Second Hospital, Dalian Medical University, Dalian, China. wqdlmu@163.com.
Dalian Medical University · CNChinese Academy of Sciences · CNPeking University · CNShanghai Jiao Tong University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The mechanism by which tumor-associated macrophages (TAMs) affect cancer progression is not fully understood. This study developed a microfluidic-based co-culture device to mimic the tumor microenvironment to assess TAM effects on invasion and metastasis in NSCLC. The results showed lung carcinoma cells could cause macrophages to show the M2 (a TAM-like) phenotype, and these M2 macrophages promoted lung cancer cell EMT and invasion. Proteomic analysis by the iTRAQ quantitation strategy and GO ontology of the cancer cells indicated that αB-Crystallin (CRYAB) might be involved in this process. Further, we confirmed the role of CRYAB in cancer invasion and metastasis through cell and animal experiments, as well as human cancer tissue assessment. Overall, we demonstrated that M2 macrophages promote malignancy in lung cancer through the EMT by upregulating CRYAB expression and activating the ERK1/2/Fra-1/slug signaling pathway.

Indexed as

Epithelial-Mesenchymal Transitionalpha-Crystallin B ChainAnimalsCarcinoma, Non-Small-Cell LungCell Line, TumorCoculture TechniquesDown-RegulationGene Knockdown TechniquesHumansMacrophagesMiceMice, NudeMicrofluidicsNeoplasm InvasivenessNeoplasm MetastasisProteomicsalpha-Crystallin B ChainCRYAB protein, human

Identifiers

PMID31097690
PMCPMC6522541
OpenAlexW2945645468

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.