ElSaeed, Karim OmarShoukry, YoussefTash, Reham FathyOmar, Nesreen Nabil2019-12-012019-12-012017-061110-0362https://doi.org/10.1016/j.jnci.2017.04.001https://www.ncbi.nlm.nih.gov/pubmed/28462847Accession Number: WOS:000404955300003Introduction: Cancer cells may exhibit outsourcing of their high energy need in order to avoid the intrinsic mitochondrial apoptosis. Reduced mitochondrial respiration and accumulation of mitochondrial genome mutations are among metabolic transformations in this regard. Mitochondrial humanin (MT-RNR2) is a small peptide with anti-apoptotic activities attributed to binding some pro-apoptotic proteins. Aim of the work: The current study aims at investigating the expression of mitochondrial humanin in bladder tumor cells and the possible casting of humanin anti-apoptotic action through orchestrating some of the mitochondrial metabolic enzymes. Material and methods: Here messenger RNA of humanin, succinate dehydrogenase, glutaminase, isocitrate dehydrogenase were compared in tissues from patients with T2 bladder carcinoma in comparison to tumor associated normal tissues from the same patients. Levels of lactate and mitochondrial pyruvate carrier (MPC1) mRNA were determined to scrutinize the prevalence of aerobic glycolysis. Results: The present study found that tumor cells had suppressed aerobic glycolysis, augmented mitochondrial respiration and interrupted tricarboxylic acid cycle, all of which were suggested to serve tumor aggressiveness. MT-RNR2 was found closely related to the alterations in mitochondrial activity. Conclusion: MT-RNR2 plays its anti-apoptotic role partly by avoiding deploying energy from complete oxidation of organic compounds to inorganic wastes. Thus MT-RNR2 can potentially serve as a new biomarker in the diagnosis of bladder carcinoma especially that it is present in blood circulation. (C) 2017 National Cancer Institute, Cairo University. Production and hosting by Elsevier B.V.en-USMPC1MT-RNR2MT-RNR2Mitochondrial respirationAerobic glycolysisT2 bladder cancerFUELSArticlehttps://doi.org/10.1016/j.jnci.2017.04.001