miR‑144‑3p regulates the resistance of lung cancer to cisplatin by targeting Nrf2

Oncol Rep. 2018 Dec;40(6):3479-3488. doi: 10.3892/or.2018.6772. Epub 2018 Oct 8.

Abstract

Chemotherapeutic drug resistance is correlated with treatment failure and poor prognosis among lung cancer patients. Numerous studies indicate the relevance of miRNAs in inducing certain drug resistance. In the course of the study, we unexpectedly found that miR‑144‑3p could regulate the cisplatin resistance of lung cancer cells via Nrf2. However, Nrf2 also could reverse activate the expression of miR‑144‑3p by binding to the ARE box in the miR‑144‑3p promoter. This may be a self‑protection mechanism of the body. In addition, we also found that in other cancer cell lines, such as HepG2, miR‑144‑3p also had the function of regulating cisplatin resistance. These findings may provide some theoretical reference for the clinical inhibition of cisplatin resistance.

MeSH terms

  • Antineoplastic Agents / pharmacology*
  • Antineoplastic Agents / therapeutic use
  • Cell Line, Tumor
  • Cisplatin / pharmacology*
  • Cisplatin / therapeutic use
  • Datasets as Topic
  • Drug Resistance, Multiple / genetics
  • Drug Resistance, Neoplasm / genetics*
  • Gene Expression Regulation, Neoplastic
  • Humans
  • Kaplan-Meier Estimate
  • Lung / pathology
  • Lung Neoplasms / drug therapy*
  • Lung Neoplasms / genetics
  • Lung Neoplasms / mortality
  • Lung Neoplasms / pathology
  • MicroRNAs / genetics
  • MicroRNAs / metabolism*
  • NF-E2-Related Factor 2 / genetics*
  • NF-E2-Related Factor 2 / metabolism
  • Prognosis
  • Promoter Regions, Genetic / genetics
  • Signal Transduction / drug effects
  • Signal Transduction / genetics

Substances

  • Antineoplastic Agents
  • MIRN144 microRNA, human
  • MicroRNAs
  • NF-E2-Related Factor 2
  • NFE2L2 protein, human
  • Cisplatin