VA Boston Healthcare System and Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA.
Mitochondrion. 2010 Apr;10(3):243-52. doi: 10.1016/j.mito.2009.12.143. Epub 2009 Dec 21.
Cancer cells respond to unfavorable microenvironments such as nutrient limitation, hypoxia, oxidative stress, and host defense by comprehensive metabolic reprogramming. Mitochondria are linked to this complex adaptive response and emerging evidence indicates that uncoupling protein-2 (UCP2), a mitochondrial inner membrane anion carrier, may contribute to this process. Effects of UCP2 on mitochondrial bioenergetics, redox homeostasis, and oxidant production in cancer cells may modulate molecular pathways of macromolecular biosynthesis, antioxidant defense, apoptosis, cell growth and proliferation, enhancing robustness and promoting chemoresistance. Elucidation of these interactions may identify novel anti-cancer strategies.
癌细胞通过全面的代谢重编程来应对不利的微环境,如营养限制、缺氧、氧化应激和宿主防御。线粒体与这种复杂的适应性反应有关,新的证据表明,解偶联蛋白 2(UCP2),一种线粒体内膜阴离子载体,可能有助于这一过程。UCP2 对癌细胞中线粒体生物能学、氧化还原稳态和氧化剂产生的影响可能调节大分子生物合成、抗氧化防御、细胞凋亡、细胞生长和增殖的分子途径,增强其稳健性并促进化疗耐药性。阐明这些相互作用可能为新的抗癌策略提供线索。