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BMC Medicine

, 9:62

First Online: 23 May 2011Received: 22 March 2011Accepted: 23 May 2011DOI: 10.1186-1741-7015-9-62

Cite this article as: Sotgia, F., Martinez-Outschoorn, U.E. & Lisanti, M.P. BMC Med 2011 9: 62. doi:10.1186-1741-7015-9-62

Abstract

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

AbbreviationsHIF1hypoxia-inducible factor 1

MMTVmouse mammary tumor virus

PyMTpolyoma middle T antigen

ROSreactive oxygen species

SOD2superoxide dismutase 2, mitochondrial enzyme

Electronic supplementary materialThe online version of this article doi:10.1186-1741-7015-9-62 contains supplementary material, which is available to authorized users.

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Autor: Federica Sotgia - Ubaldo E Martinez-Outschoorn - Michael P Lisanti

Fuente: https://link.springer.com/







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