Journal
CURRENT DRUG TARGETS
Volume 11, Issue 12, Pages 1551-1570Publisher
BENTHAM SCIENCE PUBL LTD
DOI: 10.2174/1389450111009011551
Keywords
Heme oxygenase-1; carcinogenesis; oxidative stress; cytoprotection; angiogenesis; metastasis
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Funding
- Ministry of Science and Higher Education [N401 297835, N301 314837, 311/N-COST/2008, 347/N-INCA/2008]
- Wellcome Trust
- European Commission [COST CM0602, TD0901]
- European Union [POIG. 01.01.02-00-109/09, 02.01.00-12-064/08, 02.02.00-00-014/08]
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Heme oxygenase-1 (HO-1) degrades heme to carbon monoxide (CO), biliverdin, and ferrous iron. As HO-1 expression is highly increased by stressful conditions, the major role of the enzyme is the protection against oxidative injury. Additionally, it regulates cell proliferation, modulates inflammatory response and facilitates angiogenesis. Beneficial activities of HO-1 have been recognized in many pathological states e. g. atherosclerosis, diabetes, ischemia/reperfusion injury or organ transplantation. Interestingly HO-1 expression is very often boosted in tumor tissues and could be further elevated in response to radio-, chemo-, or photodynamic therapy. A growing body of evidence suggests that HO-1 may play a role in tumor induction and can potently improve the growth and spread of tumors. This review discusses the implications of HO-1 properties for tumor proliferation and cell death, differentiation, angiogenesis and metastasis, and tumor-related inflammation. Finally, it suggests that pharmacological agents that regulate HO activity or HO-1 gene silencing may become powerful tools for preventing the onset or progression of various cancers and sensitize them to anticancer therapies.
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