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Hindi Utility of a Novel Model of Genomic Deletion of 6-Phosphofructo-2- Kinase/Fructose-2,6-Bisphosphatase (PFKFB3) in Developing Effective Anti-Cancer Strategies
*Corresponding Author:Received Date: Oct 15, 2024 / Published Date: Nov 13, 2024
Citation: Lanceta L, Telang S (2024) Utility of a Novel Model of Genomic Deletion of 6-Phosphofructo-2-Kinase/Fructose-2,6-Bisphosphatase (PFKFB3) in Developing Effective Anti-Cancer Strategies. J Oncol Res Treat. 9:295.DOI: 10.4172/aot-1000295
Copyright: © 2024 Lanceta L, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits restricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Abstract
A metabolic shift to a high rate of glycolysis is frequently observed in tumors and provides critical biosynthetic intermediates and energy for their rapid growth. The 6-phosphofructo-2-kinase/fructose-2,6-bisphosphatases (PFKFB1-4) have been recognized as important regulators of glycolysis due to their production of fructose-2,6- bisphosphate (F26BP) which activates a rate-limiting, key glycolytic enzyme, 6-phosphofructo-1-kinase enzyme (PFK-1). Due to its high kinase activity and resultant contribution to the concentration of F26BP, the PFKFB3 isoform has been extensively interrogated and determined to play a prominent role in tumor glycolysis and growth, thereby validating it as a viable target for the development of novel inhibitors. To fully understand the function of PFKFB3 and effects of decreasing its expression, the generation and examination of a model of effective genomic PFKFB3 deletion has been a critical development. Studies conducted with this recently developed inducible model of pantissue homozygous PFKFB3 genomic deletion have demonstrated the importance of the PFKFB3 enzyme in tumor growth. Additionally, the studies detailing the examination of this model have also served to validate the on-target effects of recently developed novel antagonists of PFKFB3 and indicate important avenues for developing new strategies for the effective treatment of cancer.
