The Role of Autophagy in Cancer Radiotherapy

Curr Mol Pharmacol. 2020;13(1):31-40. doi: 10.2174/1874467212666190809154518.

Abstract

Autophagy, a pathway for lysosomal-mediated cellular degradation, is a catabolic process that recycles intracellular components to maintain metabolism and survival. It is classified into three major types: macroautophagy, microautophagy, and the chaperone-mediated autophagy (CMA). Autophagy is a dynamic and multistep process that includes four stages: nucleation, elongation, autophagosome formation, and fusion. Interestingly, the influence of autophagy in cancer development is complex and paradoxical, suppressive, or promotive in different contexts. Autophagy in cancer has been demonstrated to serve as both a tumour suppressor and promoter. Radiotherapy is a powerful and common strategy for many different types of cancer and can induce autophagy, which has been shown to modulate sensitivity of cancer to radiotherapy. However, the role of autophagy in radiation treatment is controversial. Some reports showed that the upregulation of autophagy was cytoprotective for cancer cells. Others, in contrast, showed that the induction of autophagy was advantageous. Here, we reviewed recent studies and attempted to discuss the various aspects of autophagy in response to radiotherapy of cancer. Thus, we could decrease the viability of cancer cell and increase the sensibility of cancer cells to radiation, providing a new basis for the application of autophagy in clinical tumor radiotherapy.

Keywords: Autophagy; induction; inhibition; radiosensitivity; radiotherapy..

Publication types

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

MeSH terms

  • Adenylate Kinase / physiology
  • Autophagy / genetics
  • Autophagy / physiology*
  • Autophagy / radiation effects
  • Carcinoma / pathology
  • Carcinoma / radiotherapy
  • Female
  • Glioblastoma / pathology
  • Glioblastoma / radiotherapy
  • Humans
  • Male
  • Neoplasm Proteins / physiology
  • Neoplasms / pathology
  • Neoplasms / radiotherapy*
  • Neoplastic Stem Cells / pathology
  • Neoplastic Stem Cells / radiation effects
  • Organ Specificity
  • Phosphatidylinositol 3-Kinases / physiology
  • Proto-Oncogene Proteins c-akt / physiology
  • Radiation Tolerance
  • Signal Transduction / physiology
  • TOR Serine-Threonine Kinases / physiology

Substances

  • Neoplasm Proteins
  • MTOR protein, human
  • AKT1 protein, human
  • Proto-Oncogene Proteins c-akt
  • TOR Serine-Threonine Kinases
  • Adenylate Kinase