The emerging role of microRNAs in resistance to lung cancer treatments

Cancer Treat Rev. 2015 Feb;41(2):160-9. doi: 10.1016/j.ctrv.2014.12.009. Epub 2014 Dec 23.

Abstract

One of the major challenges in the treatment of lung cancer is the development of drug resistance. This represents a major obstacle in the treatment of patients, limiting the efficacy of both conventional chemotherapy and biological therapies. Deciphering the mechanisms of resistance is critical to further understanding the multifactorial pathways involved, and in developing more specific targeted treatments. To date, numerous studies have reported the potential role of microRNAs (miRNAs) in resistance to various cancer treatments. MicroRNAs are a family of small non-coding RNAs that regulate gene expression by sequence-specific targeting of mRNAs causing translational repression or mRNA degradation. More than 1200 validated human miRNAs have been identified to date. While as little as one miRNA can regulate hundreds of targets, a single target can also be affected by multiple miRNAs. Evidence suggests that dysregulation of specific miRNAs may be involved in the acquisition of resistance to a number of cancer treatments, thereby modulating the sensitivity of cancer cells to such therapies. Therefore, targeting miRNAs may be an attractive strategy for developing novel and more effective individualized therapies, improving drug efficiency, and for predicting patient response to different treatments. In this review, we provide an overview on the role of miRNAs in resistance to current lung cancer therapies and novel biological agents.

Keywords: Cancer therapies; Chemotherapy; Lung cancer; MicroRNA; Resistance.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Angiogenesis Inhibitors / pharmacology
  • Antimetabolites, Antineoplastic / pharmacology
  • Antineoplastic Agents / pharmacology*
  • Antineoplastic Agents / therapeutic use
  • Apoptosis / drug effects
  • Apoptosis / genetics
  • Drug Resistance, Neoplasm*
  • ErbB Receptors / antagonists & inhibitors
  • Gene Expression Regulation, Neoplastic / drug effects
  • Humans
  • Lung Neoplasms / drug therapy*
  • Lung Neoplasms / genetics*
  • Lung Neoplasms / mortality
  • MicroRNAs / metabolism*
  • Platinum Compounds / pharmacology
  • Radiation Tolerance
  • Radiotherapy, Adjuvant
  • TNF-Related Apoptosis-Inducing Ligand / genetics
  • TNF-Related Apoptosis-Inducing Ligand / metabolism
  • Taxoids / pharmacology

Substances

  • Angiogenesis Inhibitors
  • Antimetabolites, Antineoplastic
  • Antineoplastic Agents
  • MicroRNAs
  • Platinum Compounds
  • TNF-Related Apoptosis-Inducing Ligand
  • TNFSF10 protein, human
  • Taxoids
  • EGFR protein, human
  • ErbB Receptors