Mitochondrial oxidative stress drives tumor progression and metastasis: should we use antioxidants as a key component of cancer treatment and prevention?

The functional role of oxidative stress in cancer pathogenesis has long been a hotly debated topic. A study published this month in BMC Cancer by Goh et al. , directly addresses this issue by using a molecular genetic approach, via an established mouse animal model of human breast cancer. More speci...

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Vydáno v:	BMC medicine Ročník 9; číslo 1; s. 62
Hlavní autoři:	Sotgia, Federica, Martinez-Outschoorn, Ubaldo E, Lisanti, Michael P
Médium:	Journal Article
Jazyk:	angličtina
Vydáno:	London BioMed Central 23.05.2011 BioMed Central Ltd BMC
Témata:	Analysis Animals Antineoplastic Agents - therapeutic use Antioxidants Antioxidants - therapeutic use Biomedicine Breast Neoplasms - drug therapy Breast Neoplasms - pathology Cancer Catalase - genetics Catalase - metabolism Commentary Complications and side effects Development and progression Disease Models, Animal Drug therapy Female Gene Expression Health aspects Humans Medicine Medicine & Public Health Mice Mitochondria - metabolism Neoplasm Metastasis - pathology Neoplasm Metastasis - prevention & control Neoplasms - drug therapy Neoplasms - pathology Oxidative Stress Prevention Protein Transport Risk factors Rodent Diseases - drug therapy Rodent Diseases - pathology United States United Kingdom Cancer Associate Fibroblast Mitochondrial Oxidative Stress Tumor Stroma Mitochondrial SOD2 Triple Negative Breast Cancer Patient
ISSN:	1741-7015, 1741-7015
On-line přístup:	Získat plný text
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Shrnutí:	The functional role of oxidative stress in cancer pathogenesis has long been a hotly debated topic. A study published this month in BMC Cancer by Goh et al. , directly addresses this issue by using a molecular genetic approach, via an established mouse animal model of human breast cancer. More specifically, alleviation of mitochondrial oxidative stress, via transgenic over-expression of catalase (an anti-oxidant enzyme) targeted to mitochondria, was sufficient to lower tumor grade (from high-to-low) and to dramatically reduce metastatic tumor burden by >12-fold. Here, we discuss these new findings and place them in the context of several other recent studies showing that oxidative stress directly contributes to tumor progression and metastasis. These results have important clinical and translational significance, as most current chemo-therapeutic agents and radiation therapy increase oxidative stress, and, therefore, could help drive tumor recurrence and metastasis. Similarly, chemo- and radiation-therapy both increase the risk for developing a secondary malignancy, such as leukemia and/or lymphoma. To effectively reduce mitochondrial oxidative stress, medical oncologists should now re-consider the use of powerful anti-oxidants as a key component of patient therapy and cancer prevention. Please see related research article: http://www.biomedcentral.com/1471-2407/11/191
Bibliografie:	ObjectType-Article-2 SourceType-Scholarly Journals-1 ObjectType-Feature-3 content type line 23 ObjectType-Commentary-1
ISSN:	1741-7015 1741-7015
DOI:	10.1186/1741-7015-9-62