Studies Conducted at European Institute of Oncology on Hypoglycemia Recently Reported (Combination of Hypoglycemia and Metformin Impairs Tumor Metabolic Plasticity and Growth By Modulating the Pp2a-gsk3 Beta-mcl-1 Axis)
Health & Medicine Daily
2019 JUN 11 (NewsRx) -- By a News Reporter-Staff News Editor at Health & Medicine Daily -- Current study results on Nutritional and Metabolic Diseases and Conditions - Hypoglycemia have been published. According to news reporting originating in Milan, Italy, by NewsRx journalists, research stated, “Tumor cells may adapt to metabolic challenges by alternating between glycolysis and oxidative phosphorylation (OXPHOS). To target this metabolic plasticity, we combined intermittent fasting, a clinically feasible approach to reduce glucose availability, with the OXPHOS inhibitor metformin.”
Financial supporters for this research include Mahlke-Obermann Stiftung, European Union, AIRC, F.W.O.-Flanders, Regione Lombardia (grant DIVA), FUV.
The news reporters obtained a quote from the research from the European Institute of Oncology, “In mice exposed to 24-h feeding/fasting cycles, metformin impaired tumor growth only when administered during fasting-induced hypoglycemia. Synergistic anti-neoplastic effects of the metformin/hypoglycemia combination were mediated by glycogen synthase kinase 3 beta (GSK3 beta) activation downstream of PP2A, leading to a decline in the pro-survival protein MCL-1, and cell death.”
According to the news reporters, the research concluded: “Mechanistically, specific activation of the PP2A-GSK3 beta axis was the sum of metformin-induced inhibition of CIP2A, a PP2A suppressor, and of upregulation of the PP2A regulatory subunit B56 delta by low glucose, leading to an active PP2A-B568 delta complex with high affinity toward GSK3 beta.”
For more information on this research see: Combination of Hypoglycemia and Metformin Impairs Tumor Metabolic Plasticity and Growth By Modulating the Pp2a-gsk3 Beta-mcl-1 Axis. Cancer Cell, 2019;35(5):798-+. Cancer Cell can be contacted at: Cell Press, 50 Hampshire St, Floor 5, Cambridge, MA 02139, USA. (Elsevier - www.elsevier.com; Cancer Cell - http://www.journals.elsevier.com/cancer-cell/)
Our news correspondents report that additional information may be obtained by contacting M. Elgendy, European Institute of Oncology, Dept. of Experimental Oncology, Ieo, Via Adamello 16, I-20139 Milan, Italy. Additional authors for this research include A. Hosseini, L. Mazzarella, R. Cazzoli, P.G. Pelicci, L. Lanfrancone, S. Minucci, M. Ciro, E. Ferrari, M. Foiani, J. Weiszmann, W. Weckwerth, G. Curigliano, A. DeCensi, B. Bonanni, A. Budillon, V. Janssens, M. Ogris and M. Baccarini.
The direct object identifier (DOI) for that additional information is: https://doi.org/10.1016/j.ccell.2019.03.007. This DOI is a link to an online electronic document that is either free or for purchase, and can be your direct source for a journal article and its citation.
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