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Carbon Monoxide Expedites Metabolic Exhaustion to Inhibit Tumor Growth

På svenska

Author

  • Barbara Wegiel
  • 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 L Persson
  • Leo E. Otterbein
Show all

Summary, in English

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. (C)2013 AACR.

Publishing year

2013

Language

English

Pages

7009-7021

Publication/Series

Cancer Research

Volume

73

Issue

23

Document type

Journal article

Publisher

American Association for Cancer Research Inc.

Topic

  • Cancer and Oncology

Status

Published

Research group

  • Pathology, Malmö
  • Urological cancer, Malmö

ISBN/ISSN/Other

  • ISSN: 1538-7445