Evidence map›Paper›PMID 24121491›Full record

ArticleCancer research2013

Carbon monoxide expedites metabolic exhaustion to inhibit tumor growth.

Barbara Wegiel, David Gallo, Eva Csizmadia, Clair Harris, John Belcher, Gregory M Vercellotti, Nuno Penacho, Pankaj Seth, Vikas Sukhatme, Asif Ahmed and 5 more

Open access · bronzeAbstract read
In one paragraph

Article in Cancer research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 140 papers.

0numbers the graph read from it
0cells of the map it votes in
140citing papers in PubMed
6.9field-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

140 citing papers in PubMed, 371 citations in OpenAlex.

  1. Trial
  2. A Metal-Free Carbon Monoxide Prodrug Suppresses Metastasis of Pancreatic and Breast Cancer.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
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80 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

15 authors at 4 institutions in 3 countries.

Barbara WegielAuthors' Affiliations: Department of Surgery, Transplant Institute, Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts; Department of Clinical Sciences, Section of Urological Cancers, School of Life and Health Sciences, Aston University, Aston Triangle, Birmingham, United Kingdom; Department of Laboratory Medicine, University Hospital Malmö, Lund University, Malmö, Sweden; and Department of Medicine and Vascular Biology Center, University of Minnesota, Minneapolis, Alfama Inc., Oeiras, Portugal.
David Gallo
Eva Csizmadia
Clair Harris
John Belcher
Gregory M Vercellotti
Nuno Penacho
Pankaj Seth
Vikas Sukhatme
Asif Ahmed
Pier Paolo Pandolfi
Leszek Helczynski
Anders Bjartell
Jenny Liao Persson
Leo E Otterbein
Beth Israel Deaconess Medical Center · USAston University · GBLund University · SEUniversity of Minnesota · US

Funding

Carbon Monoxide to Prevent Circulatory CollapseR01HL076167 · NHLBI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI OTTERBEIN, LEO E · 2004 to 2007
$1.6M
Endogenous Gas Molecules As Transcription FactorsR01GM088666 · NIGMS · BETH ISRAEL DEACONESS MEDICAL CENTER · PI OTTERBEIN, LEO E · 2009 to 2012
$1.4M
Anti-Inflammatory Effects of Carbon Monoxide in the LungR01HL071797 · NHLBI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI OTTERBEIN, LEO E · 2003 to 2006
$1.3M
Heme degradation pathway and immunomodulation in prostate cancer.R21CA169904 · NCI · BETH ISRAEL DEACONESS MEDICAL CENTER · PI WEGIEL, BARBARA · 2013 to 2014
$411k
British Heart Foundation PG/06/114British Heart Foundation RG/09/001/25940Medical Research Council G0601295Medical Research Council G0700288Medical Research Council G0701824NCI NIH HHS R21 CA169904NHLBI NIH HHS HL-071797NHLBI NIH HHS HL-076167NHLBI NIH HHS R01 HL071797NHLBI NIH HHS R01 HL076167NIGMS NIH HHS R01 GM088666
6 · The paper itself

Abstract

One classical feature of cancer cells is their metabolic acquisition of a highly glycolytic phenotype. Carbon monoxide (CO), one of the products of the cytoprotective molecule heme oxygenase-1 (HO-1) in cancer cells, has been implicated in carcinogenesis and therapeutic resistance. However, the functional contributions of CO and HO-1 to these processes are poorly defined. In human prostate cancers, we found that HO-1 was nuclear localized in malignant cells, with low enzymatic activity in moderately differentiated tumors correlating with relatively worse clinical outcomes. Exposure to CO sensitized prostate cancer cells but not normal cells to chemotherapy, with growth arrest and apoptosis induced in vivo in part through mitotic catastrophe. CO targeted mitochondria activity in cancer cells as evidenced by higher oxygen consumption, free radical generation, and mitochondrial collapse. Collectively, our findings indicated that CO transiently induces an anti-Warburg effect by rapidly fueling cancer cell bioenergetics, ultimately resulting in metabolic exhaustion.

Indexed as

AnimalsAntineoplastic AgentsCarbon MonoxideCell ProliferationCells, CulturedDrug Resistance, NeoplasmDrug SynergismEnergy MetabolismHeLa CellsHep G2 CellsHumansMiceMice, NudeMice, TransgenicNeoplasmsNIH 3T3 CellsAntineoplastic AgentsCarbon Monoxide

Identifiers

PMID24121491
PMCPMC3851591
OpenAlexW2109207908

What OpenQuestion holds

Textmetadata
LicenceTDM
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.