Role of autophagy inhibition in tumor proliferative arrest

Research output: Chapter in Book/Report/Conference proceedingChapter

Abstract

During metabolic stress, autophagy is essential to maintain cellular metabolism and homeostasis by clearing toxic wastes and recycling building blocks for biosynthesis. Cancer cells upregulate autophagy to meet high proliferation demand and tolerate stressed microenvironment. Genetically engineered mouse models for cancers demonstrate tumor-promoting role of autophagy. Autophagy supports tumor growth by limiting p53 function, maintaining functional mitochondria, supplying metabolites for tumor metabolism, inhibiting senescence, modulating p62 function, preventing diversion of tumor progression to benign oncocytomas, and suppressing immune surveillance.

Original languageEnglish (US)
Title of host publicationAutophagy
Subtitle of host publicationCancer, Other Pathologies, Inflammation, Immunity, Infection, and Aging Volume 12
PublisherElsevier
Pages261-274
Number of pages14
ISBN (Electronic)9780128121467
ISBN (Print)9780128121474
DOIs
StatePublished - Jan 1 2017

All Science Journal Classification (ASJC) codes

  • Medicine(all)
  • Immunology and Microbiology(all)

Keywords

  • Atg7
  • GEMM
  • Macroautophagy
  • Mitochondria metabolism
  • p53
  • Tumor proliferative arrest

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