MYC Expression and Metabolic Redox Changes in Cancer Cells: A Synergy Able to Induce Chemoresistance.

Abstract

Chemoresistance is due to multiple factors including the induction of a metabolic adaptation of tumor cells. In fact, in these cells, stress conditions induced by therapies stimulate a metabolic reprogramming which involves the strengthening of various pathways such as glycolysis, glutaminolysis and the pentose phosphate pathway. This metabolic reprogramming is the result of a complex network of mechanisms that, through the activation of oncogenes (i.e., MYC, HIF1, and PI3K) or the downregulation of tumor suppressors (i.e., TP53), induces an increased expression of glucose and/or glutamine transporters and of glycolytic enzymes. Therefore, in order to overcome chemoresistance, it is necessary to develop combined therapies which are able to selectively and simultaneously act on the multiple molecular targets responsible for this adaptation. This review is focused on highlighting the role of MYC in modulating the epigenetic redox changes which are crucial in the acquisition of therapy resistance.

• Authors: Barbara Marengo, Ombretta Garbarino, Andrea Speciale, Lorenzo Monteleone, Nicola Traverso, Cinzia Domenicotti
• Journal: Oxidative medicine and cellular longevity (Oxid Med Cell Longev) Vol. 2019 Pg. 7346492 ( 2019) ISSN: 1942-0994 [Electronic] United States
• PMID: 31341534 (Publication Type: Journal Article, Review)

Chemical References

• MYC protein, human
• Proto-Oncogene Proteins c-myc

Topics

• Drug Resistance, Neoplasm
• Genes, myc
• Glycolysis
• Humans
• Neoplasms (drug therapy, genetics, metabolism)
• Oxidation-Reduction
• Proto-Oncogene Proteins c-myc (biosynthesis, genetics, metabolism)