Evidence map›Paper›PMID 28423485›Full record

ArticleOncotarget2017

M2 polarization of macrophages facilitates arsenic-induced cell transformation of lung epithelial cells.

Jiajun Cui, Wenhua Xu, Jian Chen, Hui Li, Lu Dai, Jacqueline A Frank, Shaojun Peng, Siying Wang, Gang Chen

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.1field-weighted citation impact, top 25% 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

11 citing papers in PubMed, 33 citations in OpenAlex.

  1. Article
  2. Article
  3. Role of Macrophages in Air Pollution Exposure Related Asthma.International journal of molecular sciences · 2022
    Review
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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 4 institutions in 2 countries.

Jiajun CuiDepartment of Biochemistry, Medical College of Yichun University, Yichun, Jiangxi 336000, China.
Wenhua XuDepartment Pharmacology & Nutritional Sciences, University of Kentucky College of Medicine, Lexington, KY 40536, USA.
Jian ChenDepartment of Ultrasound, The First Affiliated Hospital of Xiamen University, Xiamen, Fujian 361001, China.
Hui LiDepartment Pharmacology & Nutritional Sciences, University of Kentucky College of Medicine, Lexington, KY 40536, USA.
Lu DaiDepartment of Toxicology & Cancer Biology, University of Kentucky College of Medicine, Lexington, KY 40536, USA.
Jacqueline A FrankDepartment Pharmacology & Nutritional Sciences, University of Kentucky College of Medicine, Lexington, KY 40536, USA.
Shaojun PengDepartment of Biochemistry, Medical College of Yichun University, Yichun, Jiangxi 336000, China.
Siying WangDepartment of Pathophysiology, School of Basic Medicine, Anhui Medical University, Hefei, Anhui 230032, China.
Gang ChenDepartment Pharmacology & Nutritional Sciences, University of Kentucky College of Medicine, Lexington, KY 40536, USA.
University of Kentucky · USAnhui Medical University · CNFirst Affiliated Hospital of Xiamen University · CNYichun University · CN

Funding

University of Kentucky Markey Cancer Center Support Grant ECIA SupplementP30CA177558 · NCI · UNIVERSITY OF KENTUCKY · PI KATHLEEN L. O'CONNOR · 2013 to 2026
$38.3M
NCI NIH HHS P30 CA177558
6 · The paper itself

Abstract

The alterations in microenvironment upon chronic arsenic exposure may contribute to arsenic-induced lung carcinogenesis. Immune cells, such as macrophages, play an important role in mediating the microenvironment in the lungs. Macrophages carry out their functions after activation. There are two activation status for macrophages: classical (M1) or alternative (M2); the latter is associated with tumorigenesis. Our previous work showed that long-term arsenic exposure induces transformation of lung epithelial cells. However, the crosstalk between epithelial cells and macrophages upon arsenic exposure has not been investigated. In this study, using a co-culture system in which human lung epithelial cells are cultured with macrophages, we determined that long-term arsenic exposure polarizes macrophages towards M2 status through ROS generation. Co-culture with epithelial cells further enhanced the polarization of macrophages as well as transformation of epithelial cells, while blocking macrophage M2 polarization decreased the transformation. In addition, macrophage M2 polarization decreased autophagy activity, which may account for increased cell transformation of epithelial cells with co-culture of macrophages.

Indexed as

ArsenicBlotting, WesternCell DifferentiationCells, CulturedCell Transformation, NeoplasticCoculture TechniquesFlow CytometryHumansLung NeoplasmsMacrophage ActivationReal-Time Polymerase Chain ReactionRespiratory MucosaArsenicarseniclung cancermacrophagetransformation

Identifiers

PMID28423485
PMCPMC5400592
OpenAlexW2588317264

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.