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Updated: Jun 5, 2026

Measurement of Heme Synthesis Levels in Mammalian Cells
Published on: July 9, 2015
Increased levels of plasma haemoxygenase-1 in prostate cancer
A D Blann1, B Balakrishnan, P Ryan
1Haemostasis, Thrombosis and Vascular Biology Unit, University of Birmingham Centre for Cardiovascular Sciences, Birmingham, UK. a.blann@bham.ac.uk
Angiogenesis, a key component of cancer, may be driven by angiogenic growth factors, such as vascular endothelial growth factor (VEGF) and angiopoietin-2. Haemoxygenase-1 (HO-1), a haem-degrading enzyme, may have alternative roles in angiogenesis. Levels of plasma HO-1 have not been reported in prostate cancer. We tested the hypothesis of abnormal HO-1 in 30 men with early prostate cancer, compared with 22 men with benign prostate disease (BPD) and 26 men free of prostate disease, and that HO-1 levels would correlate with VEGF, angiopoietin-2, von Willebrand factor (vWf, marking endothelial perturbation) and PSA. Plasma HO-1 was twofold higher in prostate cancer than in the two control groups, while vWf, VEGF and PSA were also raised (all P<0.02). In the subjects free of prostate disease and in the BPD groups, HO-1 correlated significantly with VEGF (r>0.5, P<0.02) but the correlation in prostate cancer was not significant (r=0.117, P=0.537). There were no correlations with PSA or the Gleason stage. We conclude that HO-1 is associated with VEGF in health and BPD, but in the presence of prostate cancer, raised levels of both HO-1 and VEGF fail to correlate. This observation may have implications for the pathogenesis of prostate cancer.
Angiogenesis, a key component of cancer, may be driven by angiogenic growth factors, such as vascular endothelial growth factor (VEGF) and angiopoietin-2. Haemoxygenase-1 (HO-1), a haem-degrading enzyme, may have alternative roles in angiogenesis. Levels of plasma HO-1 have not been reported in prostate cancer. We tested the hypothesis of abnormal HO-1 in 30 men with early prostate cancer, compared with 22 men with benign prostate disease (BPD) and 26 men free of prostate disease, and that HO-1 levels would correlate with VEGF, angiopoietin-2, von Willebrand factor (vWf, marking endothelial perturbation) and PSA. Plasma HO-1 was twofold higher in prostate cancer than in the two control groups, while vWf, VEGF and PSA were also raised (all P<0.02). In the subjects free of prostate disease and in the BPD groups, HO-1 correlated significantly with VEGF (r>0.5, P<0.02) but the correlation in prostate cancer was not significant (r=0.117, P=0.537). There were no correlations with PSA or the Gleason stage. We conclude that HO-1 is associated with VEGF in health and BPD, but in the presence of prostate cancer, raised levels of both HO-1 and VEGF fail to correlate. This observation may have implications for the pathogenesis of prostate cancer.
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