The role of autophagy in escaping therapy-induced polyploidy/senescence

Adv Cancer Res. 2021:150:209-247. doi: 10.1016/bs.acr.2021.01.004. Epub 2021 Mar 11.

Abstract

Autophagy is an evolutionarily conserved process necessary to maintain cell homeostasis in response to various forms of stress such as nutrient deprivation and hypoxia as well as functioning to remove damaged molecules and organelles. The role of autophagy in cancer varies depending on the stage of cancer. Cancer therapeutics can also simultaneously evoke cancer cell senescence and ploidy increase. Both cancer cell senescence and polyploidization are reversible by depolyploidization giving rise to the progeny. Autophagy activation may be indispensable for cancer cell escape from senescence/polyploidy. As cancer cell polyploidy is proposed to be involved in cancer origin, the role of autophagy in polyploidization/depolyploidization of senescent cancer cells seems to be crucial. Accordingly, this review is an attempt to understand the complicated interrelationships between reversible cell senescence/polyploidy and autophagy.

Keywords: Autophagy; Cancer life cycle; Cancer origin; Polyploidization/depolyploidization; Therapy-induced senescence; mTOR.

Publication types

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

MeSH terms

  • Animals
  • Autophagy / physiology*
  • Cellular Senescence / drug effects
  • Cellular Senescence / genetics
  • Cellular Senescence / physiology*
  • Drug Resistance, Neoplasm* / genetics
  • Drug Resistance, Neoplasm* / physiology
  • Humans
  • Neoplasms / drug therapy
  • Neoplasms / genetics
  • Neoplasms / pathology
  • Polyploidy*