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• W2519494052 abstract "Mitochondria are important and necessary components of cell organelles. In recent times, mitochondrial metabolism has regained attention due to the growing evidence suggesting that dysfunction of mitochondria could play a major role in cancer. Cancer cells that are actively proliferating have great demand for ATP. This huge demand for ATP is met by glycolysis, which is called the ‘Warburg Effect’. Although the Warburg effect has lately been challenged, dysfunction of the mitochondrial dependent processes is a characteristic feature of almost all tumor cells, which lead to higher oxidative stress, inhibition of apoptosis and enhanced cell proliferation; which are the hallmarks of tumor cells. Mitochondrial uncoupling proteins have gained enormous interest in the field of cancer metabolism due to their impact on mitochondrial dependent processes. Uncoupling proteins are a family of mitochondrial proteins present in the inner mitochondrial membrane whose physiological role is to decrease membrane potential and hence ATP production. One of the most interesting functions of UCPs is to decrease the generation of ROS. However, because of altered mitochondrial dependent processes, cancer cells have elevated levels of ROS production leading to a phenomenon called ‘oxidative stress’. To fight against this oxidative stress, UCP2 (a homologue of UCP family) has shown to be up-regulated in a number of human cancers. However, there is no direct evidence supporting UCP2 contributes to carcinogenesis. Considering this ability of UCP2 to modulate ROS, membrane potential and mitochondrial bioenergetics, an interesting question to us, was whether UCP2 is involved in the progression of cancer. Using UCP2 homozygous knockout mice and UCP2 overexpressed cells; our data have demonstrated that knockout of UCP2 suppressed skin carcinogenesis. Overexpression of UCP2 enhanced skin cell transformation and oncogenic activation. In addition, genipin, a known UCP2 inhibitor, was able to inhibit oncogenic activation during skin cell transformation, even in UCP2 overexpressed cells. Finally, although knockout of UCP2 increased the basal levels of protein oxidation, it did not enhance protein oxidation in mouse skin epidermal tissues during skin carcinogenesis. In summary, our data have provided direct evidence that UCP2 promotes carcinogenesis, and targeting UCP2 may serve as a translational approach for chemoprevention. Citation Format: Annapoorna Sreedhar, Chunjing Zhang, Yunfeng Zhao. Knockout of UCP2 suppresses skin carcinogenesis. [abstract]. In: Proceedings of the 106th Annual Meeting of the American Association for Cancer Research; 2015 Apr 18-22; Philadelphia, PA. Philadelphia (PA): AACR; Cancer Res 2015;75(15 Suppl):Abstract nr 3053. doi:10.1158/1538-7445.AM2015-3053" @default.
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• W2519494052 date "2015-08-01" @default.
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• W2519494052 title "Abstract 3053: Knockout of UCP2 suppresses skin carcinogenesis" @default.
• W2519494052 doi "https://doi.org/10.1158/1538-7445.am2015-3053" @default.
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