Heme oxygenase-1 in tumors: Is it a false friend?

被引：330

作者：

Jozkowicz, Alicja ^{[1
]}

Was, Halina ^{[1
]}

Dulak, Jozef ^{[1
]}

机构：

[1] Jagiellonian Univ, Fac Biophys Biochem & Biotechnol, Dept Med Biotechnol, PL-30387 Krakow, Poland

来源：

ANTIOXIDANTS & REDOX SIGNALING | 2007年 / 9卷 / 12期

基金：

英国惠康基金;

关键词：

D O I：

10.1089/ars.2007.1659

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Heme oxygenase-1 (HO-1) catalyzes the oxidation of heme to biologically active products: carbon monoxide (CO), biliverdin, and ferrous iron. It participates in maintaining cellular homeostasis and plays an important protective role in the tissues by reducing oxidative injury, attenuating the inflammatory response, inhibiting cell apoptosis, and regulating cell proliferation. HO-1 is also an important proangiogenic mediator. Most studies have focused on the role of HO-1 in cardiovascular diseases, in which its significant, beneficial activity is well recognized. A growing body of evidence indicates, however, that HO-1 activation may play a role in carcinogenesis and can potently influence the growth and metastasis of tumors. HO- 1 is very often upregulated in tumor tissues, and its expression is further increased in response to therapies. Although the exact effect can be tissue specific, HO-1 can be regarded as an enzyme facilitating tumor progression. Accordingly, inhibition of HO-1 can be suggested as a potential therapeutic approach sensitizing tumors to radiation, chemotherapy, or photodynamic therapy.

引用

页码：2099 / 2117

页数：19

共 177 条

[1] Tumor stromal-derived factor-1 recruits vascular progenitors to mitotic neovasculature, where microenvironment influences their differentiated phenotypes [J].