Cited by 270Autophagy in Disease and TherapyCell death mechanisms and regulationPhagocytosis and Immune Regulation

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Autophagy regulates selective HMGB1 release in tumor cells that are destined to die

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Thorburn, J, Horita, H, Redzic, J, Hansen, K, Frankel, A E, Thorburn, A·2009·Cell Death & Differentiation

DOI 10.1038/cdd.2008.143PMC PMC2605182

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Abstract

Macroautophagy (hereafter referred to as autophagy) can increase or decrease the amount of cell death in response to various stimuli. To test whether autophagy also controls the characteristics associated with dying cells, we studied tumor cell killing by epidermal growth factor receptor-targeted diphtheria toxin (DT-EGF). DT-EGF kills epithelial and glioblastoma tumor cells with similar efficiency but by different mechanisms that depend on whether the cells activate autophagy when treated with the drug. Dying cells in which autophagy is induced selectively release the immune modulator high-mobility group B1 (HMGB1) without causing lysis of the cell membrane and classical necrosis. Conversely, cells that are killed by DT-EGF where autophagy is blocked, activate caspases but retain HMGB1. These data suggest that it may be feasible to manipulate the immunogenicity of dying cells by increasing or decreasing autophagy.

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Self-citation
Isoglycyrrhizinate Magnesium Enhances Hepatoprotective Effect of FK506 on Ischemia-Reperfusion Injury Through HMGB1 Inhibition in a Rat Model of Liver Transplantation
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Authors: Thorburn, J., Horita, H., Redzic, J., Hansen, K., Frankel, A. E., & Thorburn, A.
Affiliations: University of Colorado Anschutz (US)
Baylor Scott & White Health (US)
Corresponding author: Thorburn, A
ORCID: Hansen, K
Frankel, A E
Thorburn, A
Venue: Cell Death & Differentiation
Publisher: Springer Science and Business Media LLC
Published: 2008-10-10
Volume: 16
Issue: 1
Pages: 175-183
ISSN: 1350-9047 (ISSN-L)
1476-5403
DOI: 10.1038/cdd.2008.143
PMC: PMC2605182
OpenAlex: W2080208339
Cited by: 268
References: 43
Citations by year: 2026: 6 · 2025: 11 · 2024: 8 · 2023: 17 · 2022: 16 · 2021: 19 · 2020: 16 · 2019: 13 · 2018: 14 · 2017: 19 · 2016: 22 · 2015: 17 · 2014: 19 · 2013: 18 · 2012: 11
FWCI: 10.39
Type: journal article
Language: en
Open access: bronze
doi.org
Licence: www.springer.com/tdm (tdm)
Locations: Cell Death and Differentiation (publishedVersion)
PubMed (publishedVersion)
PubMed Central (acceptedVersion)
Funders: University of California, San Francisco
National Cancer Institute (CA111421, R01CA111421, P30CA046934)
Topics: Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Autophagy in Disease and Therapy
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
Life Sciences › Immunology and Microbiology › Immunology › Phagocytosis and Immune Regulation
Keywords: autophagy, HMGB1, cancer cell death, diphtheria toxin, epidermal growth factor receptor, glioblastoma, epithelial cancer cells, caspase activation, immunogenic cell death, tumor immunology
MeSH terms: Autophagy, Diphtheria Toxin, Epidermal Growth Factor, Glioblastoma, Humans, Immunologic Factors, Neoplasm Proteins, Neoplasms, Glandular and Epithelial, Recombinant Fusion Proteins, HMGB1 Protein, Cell Line, Tumor

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Autophagy regulates selective HMGB1 release in tumor cells that are destined to die

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