The redox protein HMGB1 regulates cell death and survival in cancer treatment

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

Research output: Contribution to journalComment/debatepeer-review

86 Scopus citations


Metabolic and therapeutic stress activates several signal transduction pathways and releases damageassociated molecular pattern molecules (DAMPs) that regulate cell death and cell survival. The prototypical DAMP, high-mobility group box 1 protein (HMGB1) is released with sustained autophagy, late apoptosis and necrosis. Our recent findings reveal that the HMGB1 protein triggers autophagy or apoptosis in cancer cells, depending on its redox status. Reducible HMGB1 binds to the receptor for advanced glycation end products (RAGE), induces Beclin 1-dependent autophagy and promotes pancreatic or colon tumor cell line resistance to chemotherapeutic agents or ionizing radiation. In contrast, oxidized HMGB1 increases the cytotoxicity of these agents and induces apoptosis via the mitochondrial pathway. This suggests a new function for HMGB1 within the tumor microenvironment, regulating cell death and survival and suggests that it plays an important functional role in cross-regulating apoptosis and autophagy.

Original languageEnglish (US)
Pages (from-to)1181-1183
Number of pages3
Issue number8
StatePublished - Nov 16 2010
Externally publishedYes


  • Apoptosis
  • Autophagy
  • Beclin 1
  • Cancer
  • Chemotherapy
  • DAMP
  • HMGB1
  • Necrosis
  • RAGE
  • Redox

ASJC Scopus subject areas

  • Molecular Biology
  • Cell Biology


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