Targeting DNA Damage Response in the Radio(Chemo)therapy of Non-Small Cell Lung Cancer

Int J Mol Sci. 2016 May 31;17(6):839. doi: 10.3390/ijms17060839.

Abstract

Lung cancer is the leading cause of cancer death worldwide due to its high incidence and mortality. As the most common lung cancer, non-small cell lung cancer (NSCLC) is a terrible threat to human health. Despite improvements in diagnosis and combined treatments including surgical resection, radiotherapy and chemotherapy, the overall survival for NSCLC patients still remains poor. DNA damage is considered to be the primary cause of lung cancer development and is normally recognized and repaired by the intrinsic DNA damage response machinery. The role of DNA repair pathways in radio(chemo)therapy-resistant cancers has become an area of significant interest in the clinical setting. Meanwhile, some studies have proved that genetic and epigenetic factors can alter the DNA damage response and repair, which results in changes of the radiation and chemotherapy curative effect in NSCLC. In this review, we focus on the effect of genetic polymorphisms and epigenetic factors such as miRNA regulation and lncRNA regulation participating in DNA damage repair in response to radio(chemo)therapy in NSCLC. These may provide novel information on the radio(chemo)therapy of NSCLC based on the individual DNA damage response.

Keywords: DNA damage and repair; epigenetics; genetic polymorphisms; non-small cell lung cancer; radiotherapy and chemotherapy; resistance.

Publication types

  • Review

MeSH terms

  • Carcinoma, Non-Small-Cell Lung / genetics
  • Carcinoma, Non-Small-Cell Lung / therapy*
  • Chemoradiotherapy
  • DNA Damage
  • DNA Repair*
  • Drug Resistance, Neoplasm
  • Epigenesis, Genetic*
  • Humans
  • Lung Neoplasms / genetics
  • Lung Neoplasms / therapy*
  • MicroRNAs / genetics
  • Polymorphism, Genetic*
  • RNA, Long Noncoding
  • Treatment Outcome

Substances

  • MicroRNAs
  • RNA, Long Noncoding