Evidence map›Paper›PMID 26359357›Full record

ArticleOncotarget2015

Cyclooxygenase-2 in tumor-associated macrophages promotes breast cancer cell survival by triggering a positive-feedback loop between macrophages and cancer cells.

Hongzhong Li, Bing Yang, Jing Huang, Yong Lin, Tingxiu Xiang, Jingyuan Wan, Hongyuan Li, Salem Chouaib, Guosheng Ren

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed, 1 pooled it
8.2field-weighted citation impact, top 2% 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

49 citing papers in PubMed, 1 synthesis or guideline pooled it, 78 citations in OpenAlex.

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  17. Metabolism in tumor-associated macrophages.International review of cell and molecular biology · 2022
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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 3 institutions in 2 countries.

Hongzhong LiChongqing Key Laboratory of Molecular Oncology and Epigenetics, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China.
Bing YangChongqing Key Laboratory of Molecular Oncology and Epigenetics, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China.
Jing HuangChongqing Key Laboratory of Molecular Oncology and Epigenetics, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China.
Yong LinChongqing Key Laboratory of Molecular Oncology and Epigenetics, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China.
Tingxiu XiangChongqing Key Laboratory of Molecular Oncology and Epigenetics, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China.
Jingyuan WanDepartment of Pharmacology, Chongqing Medical University, Chongqing, China.
Hongyuan LiChongqing Key Laboratory of Molecular Oncology and Epigenetics, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China.
Salem ChouaibUnite INSERM U753, Institut de Cancerologie Gustave Roussy, Paris, France.
Guosheng RenChongqing Key Laboratory of Molecular Oncology and Epigenetics, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China.
Chongqing Medical University · CNFirst Affiliated Hospital of Chongqing Medical University · CNInserm · FR

Funding

Impact of Prenatal Alcohol Exposure on Receptor Targeting and FunctioningR03AA020101 · NIAAA · UNIVERSITY OF NEW MEXICO HEALTH SCIS CTR · PI CALDWELL, KEVIN K. · 2010 to 2011
$148k
NIAAA NIH HHS R03 AA020101
6 · The paper itself

Abstract

Tumor-associated macrophages (TAMs) play an important role in cancer cell survival, however, the mechanism of which remains elusive. In this study, we found that COX-2 was abundantly expressed in breast TAMs, which was correlated to poor prognosis in breast cancer patients. Ectopic over-expression of COX-2 in TAMs enhanced breast cancer cell survival both in vitro and in vivo. COX-2 in TAMs was determined to be essential for the induction and maintenance of M2-phenotype macrophage polarity. COX-2(+) TAMs promoted breast cancer cell proliferation and survival by increasing Bcl-2 and P-gp and decreasing Bax in cancer cells. Furthermore, COX-2 in TAMs induced the expression of COX-2 in breast cancer cells, which in turn promoted M2 macrophage polarization. Inhibiting PI3K/Akt pathway in cancer cells suppressed COX-2(+) TAMs-induced cancer cell survival. These findings suggest that COX-2, functions as a key cancer promoting factor by triggering a positive-feedback loop between macrophages and cancer cells, which could be exploited for breast cancer prevention and therapy.

Indexed as

Feedback, PhysiologicalAnimalsAntineoplastic AgentsApoptosis Regulatory ProteinsBlotting, WesternBreast NeoplasmsCell LineCell Line, TumorCells, CulturedCell SurvivalCoculture TechniquesCyclooxygenase 2FemaleGene Expression Regulation, NeoplasticHumansMacrophagesAntineoplastic AgentsApoptosis Regulatory ProteinsCyclooxygenase 2Phosphatidylinositol 3-Kinasesbreast cancercyclooxygenase-2macrophagesprostaglandin E2tumor microenvironment

Identifiers

PMID26359357
PMCPMC4745752
OpenAlexW2162381561

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.