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2000
Volume 11, Issue 12
  • ISSN: 1389-4501
  • E-ISSN: 1873-5592

Abstract

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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/content/journals/cdt/10.2174/138945010793177906
2010-12-01
2025-04-18
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  • Article Type:
    Research Article
Keyword(s): 4-methylnitrosamino-1-(3-pyridyl)-1-butanone (NNK); activator protein-1 (AP-1); aneuploidy; angiogenesis; anticancer therapies; anticancerogenic polyphenol; APOPTOSIS; apoptotic/necrotic cell death; astroglia; atherosclerosis; basic fibroblast growth factor (bFGF); biliverdin; biliverdin reductase (BvR); c-Jun N-terminal kinase; carbon monoxide (CO); carcinogenesis; cerebellum; cobalt protoporphyrin-IX (CoPPIX); colony-stimulating factor (GMCSF); cyclin-dependent kinase (Cdk); cytoprotection; CYTOPROTECTION; cytotoxicity; desferroxamine (DFO); diabetes; dimethyl sulfoxide (DMSO); endothelial progenitor cells (EPC); epigallocatechin 3-gallate (EGCG); ferriporphyrins; ferrohemoglobin; ferrous iron; glucoronidated; haematopoietic; haptoglobin; Heme oxygenase-1; hemopexin; hepatocarcinogenesis; heterozygosity; hormonerefractory prostate cancer (HRPCA); human gliomas; interleukin-1β (IL-1β); iron regulatory proteins (IRP1; ischemia/reperfusion injury; Kaposi sarcoma; keratinocytes; lipopolysaccharide (LPS); localized prostate cancer (PCA); lymphadenopathy; lymphosarcoma; macrophage inflammatory protein-1β (MIP-1β); malignancy; matrix metalloproteinase-1 (MMP-1); mesenchymal stem cells (MSC); mesoporphyrin-IX; metastasis; myelogenous leukemia cells; namely a-fetoprotein (AFP), Wilm's tumor protein-1 (WT-1); Oncogenes; oral squamous cell carcinoma (OSCC); oxidative injury; oxidative stress; photodynamic therapy; Purkinje cells; reactive oxygen species (ROS); retinoblastoma protein (Rb); serine/threonine kinases; soluble guanylyl cyclase (sGC); Sp1 (Stimulatory protein-1); splenomegaly; Squamous carcinoma; stroma cell-derived growth factor-1 (SDF-1); superoxide dismutase (SOD); telomerase reverse transcriptase (TERT); thymidyne phosphorylase (TP); tin mesoporphyrin-IX (SnMPIX; toll-like receptor-4 (TLR4); transferrin receptor (TfR); TUMOR CELL PROLIFERATION; tumor necrosis factor (TNF); Tumor-associated angiogenic factors; UDPglucuronyl transferase; vascular endothelial growth factor (VEGF); vascular smooth muscle cells (VSMC); viral G protein-coupled receptor (vGPCR); ZnPPIX-poly ZnPPIX-polyethylene glycol (ZnPPIX-PEG)
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