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1. MUC1 and HIF-1alpha Signaling Crosstalk Induces Anabolic Glucose Metabolism to Impart Gemcitabine Resistance to Pancreatic Cancer.

Author

Shukla SK, Purohit V, Mehla K, Gunda V, Chaika NV, Vernucci E, King RJ, Abrego J, Goode GD, Dasgupta A, Illies AL, Gebregiworgis T, Dai B, Augustine JJ, Murthy D, Attri KS, Mashadova O, Grandgenett PM, Powers R, Ly QP, Lazenby AJ, Grem JL, Yu F, Matés JM, Asara JM, Kim JW, Hankins JH, Weekes C, Hollingsworth MA, Serkova NJ, Sasson AR, Fleming JB, Oliveto JM, Lyssiotis CA, Cantley LC, Berim L, and Singh PK

Published
2017
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2. MUC1 and HIF-1alpha Signaling Crosstalk Induces Anabolic Glucose Metabolism to Impart Gemcitabine Resistance to Pancreatic Cancer.

Author

Shukla SK, Purohit V, Mehla K, Gunda V, Chaika NV, Vernucci E, King RJ, Abrego J, Goode GD, Dasgupta A, Illies AL, Gebregiworgis T, Dai B, Augustine JJ, Murthy D, Attri KS, Mashadova O, Grandgenett PM, Powers R, Ly QP, Lazenby AJ, Grem JL, Yu F, Matés JM, Asara JM, Kim JW, Hankins JH, Weekes C, Hollingsworth MA, Serkova NJ, Sasson AR, Fleming JB, Oliveto JM, Lyssiotis CA, Cantley LC, Berim L, and Singh PK

Subjects
Carbon metabolism, Deoxycytidine therapeutic use, Digoxin pharmacology, Humans, Hypoxia-Inducible Factor 1, alpha Subunit antagonists & inhibitors, Pancreatic Neoplasms genetics, Pancreatic Neoplasms metabolism, Pentose Phosphate Pathway, Prognosis, Pyrimidines biosynthesis, Signal Transduction, Gemcitabine, Deoxycytidine analogs & derivatives, Drug Resistance, Neoplasm, Glucose metabolism, Hypoxia-Inducible Factor 1, alpha Subunit metabolism, Mucin-1 metabolism, Pancreatic Neoplasms drug therapy
Abstract

Poor response to cancer therapy due to resistance remains a clinical challenge. The present study establishes a widely prevalent mechanism of resistance to gemcitabine in pancreatic cancer, whereby increased glycolytic flux leads to glucose addiction in cancer cells and a corresponding increase in pyrimidine biosynthesis to enhance the intrinsic levels of deoxycytidine triphosphate (dCTP). Increased levels of dCTP diminish the effective levels of gemcitabine through molecular competition. We also demonstrate that MUC1-regulated stabilization of hypoxia inducible factor-1α (HIF-1α) mediates such metabolic reprogramming. Targeting HIF-1α or de novo pyrimidine biosynthesis, in combination with gemcitabine, strongly diminishes tumor burden. Finally, reduced expression of TKT and CTPS, which regulate flux into pyrimidine biosynthesis, correlates with better prognosis in pancreatic cancer patients on fluoropyrimidine analogs., (Copyright © 2017 Elsevier Inc. All rights reserved.)

Published
2017
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