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Erschienen in: Virchows Archiv 5/2005

01.05.2005 | Original Article

Heme oxygenase-1 accelerates protumoral effects of nitric oxide in cancer cells

verfasst von: Takamitsu Sasaki, Kazuhiro Yoshida, Hideaki Kondo, Hitoshi Ohmori, Hiroki Kuniyasu

Erschienen in: Virchows Archiv | Ausgabe 5/2005

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Abstract

We examined the biological effects of nitric oxide (NO) and its mediator, heme oxygenase-1 (HO-1), in cancer. Urogenital cancer cell lines, SKRC, T24 and DU145, were treated with various concentrations of sodium nitroprusside (SNP), a NO donor. The medium nitrite concentration was exponentially increased according to the concentration of SNP. Cell growth inhibition by NO was observed only at high nitrite concentrations (>20 μM) in DU145 and T24 cells. Nitrite did not inhibit the growth of SKRC cells at any of the concentrations used. Doxorubicin (DXR) inhibited cell growth in the three cell lines, whereas growth inhibition recovered in the presence of <10 μM nitrite. The recovery of DXR-induced growth inhibition was closely associated with an increase in Bcl-2 in the presence of <10 μM nitrite. Vascular endothelial growth factor (VEGF) secretion was also increased in the presence of <10 and <20 μM nitrite, respectively, in DU145 and SKRC or T24 cells. The expression of HO-1 was associated with sensitivity to NO-induced growth inhibition at constitutive levels, and was induced by SNP treatment. HO-1 inhibition by HO-1 antisense S-oligodeoxynucleotide treatment increased NO-induced growth inhibition, and decreased Bcl-2 expression or VEGF secretion in the three cell lines. These findings suggest that the NO/HO-1 system has protumoral effects.
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Metadaten
Titel
Heme oxygenase-1 accelerates protumoral effects of nitric oxide in cancer cells
verfasst von
Takamitsu Sasaki
Kazuhiro Yoshida
Hideaki Kondo
Hitoshi Ohmori
Hiroki Kuniyasu
Publikationsdatum
01.05.2005
Erschienen in
Virchows Archiv / Ausgabe 5/2005
Print ISSN: 0945-6317
Elektronische ISSN: 1432-2307
DOI
https://doi.org/10.1007/s00428-005-1247-x

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