Apoptosis to autophagy switch triggered by the MHC class III-encoded receptor for advanced glycation endproducts (RAGE)

Rui Kang, Daolin Tang, Michael T. Lotze, Herbert J. Zeh

Research output: Contribution to journalShort survey

31 Citations (Scopus)

Abstract

The receptor for advanced glycation end products (RAGE) is a member of the immunoglobulin gene superfamily, encoded within the major histocompatability complex class III region. Its multiple ligands include the high mobility group box 1 chromatin binding protein, HMGB1. Recently we reported that RAGE-HMGB1 critically regulates autophagy and apoptosis in pancreatic cancer cells in vivo and in vitro in response to chemotherapy. RAGE inhibits apoptosis ("programmed cell death") by a p53 transcription-independent pathway during the response to chemotherapeutic agents. RAGE sustains autophagy ("programmed cell survival") associated with decreased phosphorylation of the mammalian target of rapamycin (mTOR) and increased Beclin 1-Vps34 interaction. These findings provide insight into how autophagy- and apoptosis-crossregulatory molecules interact in response to cellular stress including tumor therapy.

Original languageEnglish (US)
Pages (from-to)91-93
Number of pages3
JournalAutophagy
Volume7
Issue number1
DOIs
StatePublished - Jan 2011
Externally publishedYes

Fingerprint

Autophagy
Apoptosis
HMGB1 Protein
Immunoglobulin Genes
Sirolimus
Pancreatic Neoplasms
Chromatin
Cell Survival
Carrier Proteins
Cell Death
Phosphorylation
Ligands
Drug Therapy
Advanced Glycosylation End Product-Specific Receptor
Neoplasms
Therapeutics

Keywords

  • Apoptosis
  • Autophagy
  • Beclin 1
  • DAMP
  • mTOR
  • p53
  • Pancreatic cancer
  • RAGE
  • vps34

ASJC Scopus subject areas

  • Molecular Biology
  • Cell Biology

Cite this

Apoptosis to autophagy switch triggered by the MHC class III-encoded receptor for advanced glycation endproducts (RAGE). / Kang, Rui; Tang, Daolin; Lotze, Michael T.; Zeh, Herbert J.

In: Autophagy, Vol. 7, No. 1, 01.2011, p. 91-93.

Research output: Contribution to journalShort survey

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