Low carbohydrate diet prevents Mcl-1-mediated resistance to BH3-mimetics

Oncotarget. 2016 Nov 8;7(45):73270-73279. doi: 10.18632/oncotarget.12309.

Abstract

Overexpression of Mcl-1 is implicated in resistance of several cancers to chemotherapeutic treatment, therefore identifying a safe way to decrease its expression in tumor cells represents a central goal. We investigated if a modulation of the diet could impact on Mcl-1 expression using a Myc-driven lymphoma model. We established that a partial reduction of caloric intake by 25% represents an efficient way to decrease Mcl-1 expression in tumor cells. Furthermore, using isocaloric custom diets, we observed that carbohydrates (CHO) are the main regulators of Mcl-1 expression within the food. Indeed, feeding lymphoma-bearing mice with a diet having 25% less carbohydrates was sufficient to decrease Mcl-1 expression by 50% in lymphoma cells. We showed that a low CHO diet resulted in AMPK activation and mTOR inhibition leading to eukaryotic elongation factor 2 (eEF2) inhibition, blocking protein translation elongation. Strikingly, a low CHO diet was sufficient to sensitize Myc-driven lymphoma-bearing mice to ABT-737-induced cell death in vivo. Thus reducing carbohydrate intake may represent a safe way to decrease Mcl-1 expression and to sensitize tumor cells to anti-cancer therapeutics.

Keywords: Mcl-1; cancer; low carbohydrate diet; metabolism; resistance to treatment.

MeSH terms

  • AMP-Activated Protein Kinases / metabolism
  • Animals
  • Biological Mimicry*
  • Biphenyl Compounds / pharmacology
  • Cell Line, Tumor
  • Cell Survival / drug effects
  • Diet, Carbohydrate-Restricted*
  • Disease Models, Animal
  • Drug Resistance, Neoplasm / genetics
  • Heterografts
  • Humans
  • Lymphoma / drug therapy
  • Lymphoma / genetics
  • Lymphoma / metabolism
  • Lymphoma / pathology
  • Mice
  • Myeloid Cell Leukemia Sequence 1 Protein / chemistry
  • Myeloid Cell Leukemia Sequence 1 Protein / genetics
  • Myeloid Cell Leukemia Sequence 1 Protein / metabolism*
  • Nitrophenols / pharmacology
  • Peptide Fragments / pharmacology*
  • Piperazines / pharmacology
  • Protein Biosynthesis / drug effects
  • Proto-Oncogene Proteins / pharmacology*
  • Signal Transduction
  • Sulfonamides / pharmacology
  • TOR Serine-Threonine Kinases / metabolism

Substances

  • ABT-737
  • Bax protein (53-86)
  • Biphenyl Compounds
  • Myeloid Cell Leukemia Sequence 1 Protein
  • Nitrophenols
  • Peptide Fragments
  • Piperazines
  • Proto-Oncogene Proteins
  • Sulfonamides
  • TOR Serine-Threonine Kinases
  • AMP-Activated Protein Kinases