Evidence map›Paper›PMID 22534817›Full record

ArticleJournal of thoracic oncology : official publication of the International Association for the Study of Lung Cancer2012

Interleukin-17 and prostaglandin E2 are involved in formation of an M2 macrophage-dominant microenvironment in lung cancer.

Lunxu Liu, Dongxia Ge, Lin Ma, Jiandong Mei, Sen Liu, Qiuyang Zhang, Fuqiang Ren, Hu Liao, Qiang Pu, Tao Wang and 1 more

Open access · greenAbstract readComparative Study
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of thoracic oncology : official publication of the International Association for the Study of Lung Cancer, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 83 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
83citing papers in PubMed, 1 pooled it
5.0field-weighted citation impact, top 4% 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

83 citing papers in PubMed, 1 synthesis or guideline pooled it, 130 citations in OpenAlex.

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23 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 3 institutions in 2 countries.

Lunxu LiuDepartment of Thoracic Surgery, West China Hospital, Sichuan University, Chengdu, China.
Dongxia Ge
Lin Ma
Jiandong Mei
Sen Liu
Qiuyang Zhang
Fuqiang Ren
Hu Liao
Qiang Pu
Tao Wang
Zongbing You
Tulane University · USWest China Hospital of Sichuan University · CNSichuan University · CN

Funding

UNCOVERING THE MECHANISMS OF OSTEOSARCOMA METASTASIS SUPPRESSION BY MTBPP20RR020152 · NCRR · TULANE UNIVERSITY OF LOUISIANA · PI DEININGER, PRESCOTT L. · 2004 to 2011
$17.0M
Mentoring a Cancer Genetics ProgramP20GM103518 · NIGMS · TULANE UNIVERSITY OF LOUISIANA · PI DEININGER, PRESCOTT L. · 2012 to 2013
$4.3M
NCRR NIH HHS P20 RR020152NCRR NIH HHS P20RR020152NIGMS NIH HHS P20 GM103518NIGMS NIH HHS P20GM103518
6 · The paper itself

Abstract

introductionTumor-associated macrophages (TAMs) are divided into M1 and M2 macrophages. M1 macrophages inhibit tumor growth, whereas M2 macrophages promote tumor growth and metastasis. The aim of this study was to examine the possible causes leading to the formation of an M2-macrophage-dominant tumor microenvironment in non-small-cell lung cancer.

methodsForty-eight archived lung tumor samples were examined for the expression of interleukin-17 (IL-17) receptors, IL-17 receptor A (IL-17RA) and IL-17 receptor C (IL-17RC), and the number of TAMs using immunohistochemical staining. Twenty fresh lung tumors and matched normal lung tissues were examined for expression of IL-17, cyclooxygenase-2, and prostaglandin E2 (PGE2), using enzyme-linked immunosorbent assay and Western blot analysis. Macrophage-migration assays were performed using fresh lung tumor tissues and IL-17 as chemoattractants. Induction of M2-macrophage differentiation was analyzed using real-time quantitative polymerase chain reaction.

resultsTAMs expressed IL-17RA and IL-17RC. Lung tumors expressed higher levels of IL-17, cyclooxygenase-2, and PGE2, compared with normal lung tissues. Lung tumor tissues attracted migration of mouse RAW264.7 macrophages and primary peritoneal macrophages through IL-17, which was mediated by IL-17RA and IL-17RC. IL-17 did not induce either M1- or M2-macrophage differentiation. However, human lung cancer A549 cells strongly induced M2-macrophage differentiation of RAW264.7 macrophages when the two cell lines were cocultured. The inductive factor secreted by A549 cells was identified to be PGE2.

conclusionsIL-17 recruits macrophages, and PGE2 induces M2-macrophage differentiation, hence the increased levels of IL-17 and PGE2 in lung cancer contribute to the formation of an M2-macrophage-dominant tumor microenvironment.

Indexed as

Tumor MicroenvironmentAdenocarcinomaAdultAgedAged, 80 and overAnimalsApoptosisBiomarkers, TumorBlotting, WesternCarcinoma, Non-Small-Cell LungCarcinoma, Squamous CellCase-Control StudiesCell DifferentiationCell MovementCell ProliferationCyclooxygenase 2Biomarkers, TumorCyclooxygenase 2DinoprostoneIl17ra protein, mouseIl17rc protein, mouseInterleukin-17Receptors, InterleukinReceptors, Interleukin-17

Identifiers

PMID22534817
PMCPMC3378786
OpenAlexW2058034626

What OpenQuestion holds

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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.