miR-210-3p mediates metabolic adaptation and sustains DNA damage repair of resistant colon cancer cells to treatment with 5-fluorouracil

Mol Carcinog. 2019 Dec;58(12):2181-2192. doi: 10.1002/mc.23107. Epub 2019 Aug 29.

Abstract

Chemoresistance is the primary cause of chemotherapy failure. Compelling evidence shows that micro RNAs (miRNAs) contribute to reprogram cancer cells toward a resistant phenotype. We investigate the role of miRNAs in the response to acute treatment with 5-FU in colon cancer-resistant cells. We performed a global gene expression profile for the entire miRNA genome and found a change in the expression of four miRNAs following acute treatment with 5-FU. Among them, we focused on miR-210-3p, previously described as a key regulator of DNA damage repair mechanisms and mitochondrial metabolism. We show that miR-210-3p downregulation enables resistant cells to counteract the toxic effect of the drug increasing the expression of RAD-52 protein, responsible for DNA damage repair. Moreover, miR-210-3p downregulation enhances oxidative phosphorylation (OXPHOS), increasing the expression levels of succinate dehydrogenase subunits D, decreasing intracellular succinate levels and inhibiting HIF-1α expression. Altogether, these adaptations lead to increased cells survival following drug exposure. These evidence suggest that miR-210-3p downregulation following 5-FU sustains DNA damage repair and metabolic adaptation to counteract drug treatment.

Keywords: 5-fluorouracil; DNA damage; chemoresistance; miR-210-3p; oxidative phosphorylation.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adaptation, Physiological / drug effects
  • Adaptation, Physiological / genetics
  • Antimetabolites, Antineoplastic / pharmacology
  • Cell Survival / drug effects
  • Cell Survival / genetics
  • Colonic Neoplasms / genetics*
  • Colonic Neoplasms / metabolism
  • DNA Damage
  • DNA Repair*
  • Down-Regulation / drug effects
  • Drug Resistance, Neoplasm / drug effects*
  • Drug Resistance, Neoplasm / genetics
  • Fluorouracil / pharmacology*
  • Gene Expression Profiling / methods
  • Gene Expression Regulation, Neoplastic / drug effects*
  • HT29 Cells
  • Humans
  • MicroRNAs / genetics*

Substances

  • Antimetabolites, Antineoplastic
  • MIRN210 microRNA, human
  • MicroRNAs
  • Fluorouracil