Autophagy process is associated with anti-neoplastic function

Acta Biochim Biophys Sin (Shanghai). 2011 Jun;43(6):425-32. doi: 10.1093/abbs/gmr028. Epub 2011 Apr 26.

Abstract

Autophagy is a highly conserved process of cellular degradation, which is present in yeast, plants, and mammals. Under normal physiological conditions, autophagy acts to maintain cellular homeostasis and regulate the turnover of organelles. In response to cellular stresses, autophagy prevents the accumulation of impaired proteins and organelles, which serves to inhibit carcinogenesis. On this basis, it is widely accepted that most tumor suppressors, such as beclin 1 associated proteins, forkhead box class O (FoxO) family proteins, multiple mammalian target of Rapamycin (mTOR) inactivators, and nuclear p53 play a role in inducing autophagy. Here, we focus on how the process of autophagy is associated with anti-neoplastic function.

Publication types

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

MeSH terms

  • Adaptor Proteins, Signal Transducing / physiology
  • Animals
  • Apoptosis Regulatory Proteins / chemistry
  • Apoptosis Regulatory Proteins / physiology*
  • Autophagy / drug effects
  • Autophagy / physiology*
  • Beclin-1
  • Forkhead Box Protein O1
  • Forkhead Box Protein O3
  • Forkhead Transcription Factors / physiology*
  • Humans
  • Signal Transduction / physiology
  • TOR Serine-Threonine Kinases / physiology*
  • Tumor Suppressor Protein p53 / physiology
  • Tumor Suppressor Proteins / genetics
  • Tumor Suppressor Proteins / physiology*

Substances

  • Adaptor Proteins, Signal Transducing
  • Ambra1 protein, mouse
  • Apoptosis Regulatory Proteins
  • Beclin-1
  • Becn1 protein, mouse
  • FOXO1 protein, human
  • Forkhead Box Protein O1
  • Forkhead Box Protein O3
  • Forkhead Transcription Factors
  • FoxO3 protein, mouse
  • Sh3glb1 protein, mouse
  • Tumor Suppressor Protein p53
  • Tumor Suppressor Proteins
  • UVRAG protein, mouse
  • TOR Serine-Threonine Kinases