Overexpression of Heme Oxygenase-1 in Murine Melanoma

Waś, Halina; Cichoń, Tomasz; Smolarczyk, Ryszard; Rudnicka, Dominika; Stopa, Magdalena; Chevalier, Catherine; Léger, Jean J.; Lackowska, B; Grochot, Anna; Bojkowska, Karolina; Ratajska, Anna; Kiéda, Claudine; Szala, Stanisław; Dulak, Józef; Józkowicz, Alicja

doi:10.2353/ajpath.2006.051365

Cited by 176 publications

(102 citation statements)

References 81 publications

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“…Targeted inhibition of HO by polyethylene glycol-linked ZnPP showed growth inhibitory activity against solid Sarcoma-180 tumours in mice (Fang et al 2003). Precise mechanisms as to how the HO/CO system promotes tumour growth are not fully understood, but widespread processes including the induction of resistance to stress and apoptosis (Doi et al 1999;Liu et al 2004;Was et al 2006), the altered expression of cell cycle and differentiation genes Koiso et al 2000;Chauveau et al 2005;Zwerina et al 2005), and the promotion of angiogenesis (Cherrington et al 2000;Dulak et al 2002;Sunamura et al 2003;Cisowski et al 2005;Hirai et al 2007;Deshane et al 2007) have been suggested (Fig. 3).…”

Section: Ho Activation In Cancerous Conditionsmentioning

confidence: 98%

Inhibitors of the heme oxygenase – carbon monoxide system: on the doorstep of the clinic?

Kinobe

Dercho

Nakatsu

2008

Can. J. Physiol. Pharmacol.

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The past decade has seen substantial developments in our understanding of the physiology, pathology, and pharmacology of heme oxygenases (HO), to the point that investigators in the field are beginning to contemplate therapies based on administration of HO agonists or HO inhibitors. A significant amount of our current knowledge is based on the judicious application of metalloporphyrin inhibitors of HO, despite their limitations of selectivity. Recently, imidazole-based compounds have been identified as potent and more selective HO inhibitors. This 'next generation' of HO inhibitors offers a number of desirable characteristics, including isozyme selectivity, negligible effects on HO protein expression, and physicochemical properties favourable for in vivo distribution. Some of the applications of HO inhibitors that have been suggested are treatment of hyperbilirubinemia, neurodegenerative disorders, certain types of cancer, and bacterial and fungal infections. In this review, we address various approaches to altering HO activity with a focus on the potential applications of second-generation inhibitors of HO.

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Section: Ho Activation In Cancerous Conditionsmentioning

confidence: 98%

Inhibitors of the heme oxygenase – carbon monoxide system: on the doorstep of the clinic?

Kinobe

Dercho

Nakatsu

2008

Can. J. Physiol. Pharmacol.

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“…However, the abnormally elevated expression and activity of this enzyme have been often reported in several tumor tissues, which may influence cancer cell proliferation, invasion and metastasis. In line with this notion, the overexpression of HO-1 enhanced viability, proliferation, and metastatic potential of melanoma cells [13]. HO-1 also stimulates angiogenesis through upregulation of vascular endothelial growth factor and overproduction of pro-angiogenic carbon monoxide [14].…”

Section: Introductionmentioning

confidence: 99%

4-Hydroxyestradiol induces mammary epithelial cell transformation through Nrf2-mediated heme oxygenase-1 overexpression

Park

Lee

et al. 2016

Oncotarget

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Estrogen (17β-estradiol, E2) undergoes oxidative metabolism by CYP1B1 to form 4-hydroxyestradiol (4-OHE2), a putative carcinogenic metabolite of estrogen. Our previous study showed that 4-OHE2-induced production of reactive oxygen species contributed to neoplastic transformation of human breast epithelial (MCF-10A) cells. In this study, 4-OHE2, but not E2, increased the expression of heme oxygenase-1 (HO-1), a sensor and regulator of oxidative stress, in MCF-10A cells. Silencing the HO-1 gene in MCF-10A cells suppressed 4-OHE2-induced cell proliferation and transformation. In addition, subcutaneous administration of 4-OHE2 markedly enhanced the growth of the MDA-MB-231 human breast cancer xenografts, which was retarded by zinc protoporphyrin, a pharmacological inhibitor of HO-1. 4-OHE2-induced HO-1 expression was mediated by NF-E2-related factor 2 (Nrf2). We speculate that an electrophilic quinone formed as a consequence of oxidation of 4-OHE2 binds directly to Kelch-like ECH-associated protein 1 (Keap1), an inhibitory protein that sequesters Nrf2 in the cytoplasm. This will diminish association between Nrf2 and Keap1. 4-OHE2 failed to interrupt the interaction between Keap1 and Nrf2 and to induce HO-1 expression in Keap1-C273S or C288S mutant cells. Lano-LC-ESI-MS/MS analysis in MCF-10A-Keap1-WT cells which were treated with 4-OHE2 revealed that the peptide fragment containing Cys288 gained a molecular mass of 287.15 Da, equivalent to the addition of a single molecule of 4-OHE2-derived ortho-quinones.

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“…Completed physician-initiated studies with inhaled CO in human volunteers were performed in acute lung inflammation and COPD where anti-inflammatory effects were observed [79–81], but these studies did not evaluate careful dose ranging. Clearly, there is a great deal of work yet to be done to understand the therapeutic potential of HO-1 and CO in a clinically useful modality, particularly because there are a handful of reports arguing that increased inhibition of HO-1 can also be beneficial in certain cancers [82–84]. …”

Section: Discussionmentioning

confidence: 99%

The social network of carbon monoxide in medicine

Węgiel

Hanto

Otterbein

2013

Trends in Molecular Medicine

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Networking between cells is critical for proper functioning of the cellular milieu and is mediated by cascades of highly regulated and overlapping signaling molecules. The enzyme heme oxygenase-1 (HO-1) generates three separate signaling molecules through the catalysis of heme – carbon monoxide (CO), biliverdin, and iron – each of which acts via distinct molecular targets to influence cell function, both proximally and distally. This review focuses on state-of-the art developments and insights into the impact of HO-1 and CO on the innate immune response, the effects of which are responsible for an ensemble of functions that help regulate complex immunologic responses to bacterial sepsis and ischemia/reperfusion injury. HO-1 exemplifies an evolutionarily conserved system necessary for the cellular milieu to adapt appropriately, function properly, and ensure survival of the organism.

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Overexpression of Heme Oxygenase-1 in Murine Melanoma

Cited by 176 publications

References 81 publications

Inhibitors of the heme oxygenase – carbon monoxide system: on the doorstep of the clinic?

Inhibitors of the heme oxygenase – carbon monoxide system: on the doorstep of the clinic?

4-Hydroxyestradiol induces mammary epithelial cell transformation through Nrf2-mediated heme oxygenase-1 overexpression

The social network of carbon monoxide in medicine

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