Evidence map›Paper›PMID 26418896›Full record

ArticleOncotarget2015

Heme oxygenase-1 in macrophages controls prostate cancer progression.

Zsuzsanna Nemeth, Mailin Li, Eva Csizmadia, Balazs Döme, Martin Johansson, Jenny Liao Persson, Pankaj Seth, Leo Otterbein, Barbara Wegiel

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 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
2.4field-weighted citation impact, top 11% 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

39 citing papers in PubMed, 51 citations in OpenAlex.

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  13. A Coumarin-Porphyrin FRET Break-Apart Probe for Heme Oxygenase-1.Journal of the American Chemical Society · 2021
    Article
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  20. Interplay of Heme with Macrophages in Homeostasis and Inflammation.International journal of molecular sciences · 2020
    Review
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 4 countries.

Zsuzsanna NemethDepartment of Surgery, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, USA.
Mailin LiDepartment of Surgery, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, USA.
Eva CsizmadiaDepartment of Surgery, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, USA.
Balazs DömeDepartment of Tumor Biology, National Koranyi Institute of TB and Pulmonology, Budapest, Hungary.
Martin JohanssonDepartment of Laboratory Medicine, Lund University, Malmo, Sweden.
Jenny Liao PerssonDepartment of Laboratory Medicine, Lund University, Malmo, Sweden.
Pankaj SethDepartment of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, USA.
Leo OtterbeinDepartment of Surgery, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, USA.
Barbara WegielDepartment of Surgery, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, USA.
Beth Israel Deaconess Medical Center · USHarvard University · USLund University · SEOrszágos Korányi Tbc és Pulmonológiai Intézet · HU

Funding

Heme degradation pathway and immunomodulation in prostate cancer.R21CA169904 · NCI · BETH ISRAEL DEACONESS MEDICAL CENTER · PI WEGIEL, BARBARA · 2013 to 2014
$411k
NCI NIH HHS 1R21CA169904-01NCI NIH HHS R21 CA169904
6 · The paper itself

Abstract

Innate immune cells strongly influence cancer growth and progression via multiple mechanisms including regulation of epithelial to mesenchymal transition (EMT). In this study, we investigated whether expression of the metabolic gene, heme oxygenase-1 (HO-1) in tumor microenvironment imparts significant effects on prostate cancer progression.We showed that HO-1 is expressed in MARCO-positive macrophages in prostate cancer (PCa) xenografts and human prostate cancers. We demonstrated that macrophage specific (LyzM-Cre) conditional deletion of HO-1 suppressed growth of PC3 xenografts in vivo and delayed progression of prostate intraepithelial neoplasia (PIN) in TRAMP mice. However, initiation and progression of cancer xenografts in the presence of macrophages lacking HO-1 resulted in loss of E-cadherin, a known marker of poor prognosis as well as EMT. Application of CO, a product of HO-1 catalysis, increased levels of E-cadherin in the adherens junctions between cancer cells. We further showed that HO-1-driven expression of E-cadherin in cancer cells cultured in the presence of macrophages is dependent on mitochondrial activity of cancer cells.In summary, these data suggest that HO-1-derived CO from tumor-associated macrophages influences, in part, E-cadherin expression and thus tumor initiation and progression.

Indexed as

AnimalsCadherinsCell Line, TumorCell ProliferationDisease ProgressionHeme Oxygenase-1HeterograftsHumansMacrophagesMaleMembrane ProteinsMiceMice, KnockoutProstatic NeoplasmsTumor MicroenvironmentCadherinsHeme Oxygenase-1HMOX1 protein, humanHmox1 protein, mouseMembrane ProteinsE-cadherinheme oxygenase-1mitochondriatumor-associated macrophagestumor microenvironment

Identifiers

PMID26418896
PMCPMC4741794
OpenAlexW2119003936

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.