Cited by 221Autophagy in Disease and TherapyNeuroblastoma Research and TreatmentsHistone Deacetylase Inhibitors Research

Histone deacetylase 10 promotes autophagy-mediated cell survival

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Oehme, Ina, Linke, Jan-Peter, Böck, Barbara C., Milde, Till, Lodrini, Marco, Hartenstein, Bettina, Wiegand, Inga, Eckert, Christian +10 more·2013·Proceedings of the National Academy of Sciences

Abstract

Significance: Resistance to chemotherapy is one of the major challenges in oncology. Neuroblastoma is the most common extracranial solid tumor in childhood, and the successful response of high-risk patients to chemotherapy remains poor. Our work showed that the so far poorly studied histone deacetylase (HDAC)10 promotes autophagy-mediated cell survival and signals poor outcome in independent high-risk patient cohorts. Inhibition of HDAC10 sensitized tumor cells for cytotoxic drug treatment. These results offer HDAC10 as a potential biomarker for treatment response of high-risk tumors and open new avenues for developing selective treatment strategies to bypass drug resistance of these tumors.

Integrity signals

Registry

Crossref · 10.1073/pnas.1300113110

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59 of 59 references verified0 citation errors · 0 not checkable

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  • Both HDAC10 and spermidine promote cellular survival through autophagy.

    “Both HDAC10 and spermidine are known to promote cellular survival through autophagy.”
  • HDAC10 is an emerging target for treatment of advanced-stage neuroblastoma.

    “As the suppression of autophagy to sustain the cytotoxicity of chemotherapeutic drugs is a novel strategy for cancer chemotherapy3435, HDAC10 is an emerging target for the treatment of advanced-stage neuroblastoma32.”
  • HDAC10 protects cancer cells from chemotherapeutic drugs by mediating autophagy; upregulation of HDAC10 is a marker of poor outcome for advanced stage neuroblastoma patients.

    “Recently, it has been demonstrated that HDAC10 protects cancer cells from chemotherapeutic drugs by mediating auto-phagy, a survival response to the cellular damage and metabolic stress induced by cytotoxic drugs; indeed, the upregulation of HDAC10 is a marker of poor outcome for advanced stage neuroblastoma patients32.”
  • Knockdown or inhibition of HDAC10 blocks autophagy in a panel of neuroblastoma cell lines, sensitizing these cells to doxorubicin.

    “However, the knockdown or inhibition of HDAC10 blocks autophagy in a panel of neuroblastoma cells lines, thereby sensitizing these highly malignant cells to the cytotoxic drug doxorubicin32.”

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Authors
Oehme, I., Linke, J.-P., Böck, B. C., Milde, T., Lodrini, M., Hartenstein, B., Wiegand, I., Eckert, C., Roth, W., Kool, M., Kaden, S., Gröne, H.-J., Schulte, J. H., Lindner, S., Hamacher-Brady, A., Brady, N. R., Deubzer, H. E., & Witt, O.
Affiliations
  • German Cancer Research Center (DE)
  • Tech Evotec (Munich) GmbH, D-82151 Martinsried, Germany;
  • Essen University Hospital (DE)
  • Lysosomal Systems Biology, DKFZ, D-69120 Heidelberg, Germany; and
Venue
Proceedings of the National Academy of Sciences
Published
2013-06-25
Volume
110
Issue
28
Pages
E2592-601
ISSN
  • 0027-8424 (ISSN-L)
  • 1091-6490
OpenAlex
W2094205300
Cited by
221
References
59
Citations by year
2026: 15 · 2025: 18 · 2024: 10 · 2023: 9 · 2022: 24 · 2021: 25 · 2020: 22 · 2019: 18 · 2018: 17 · 2017: 18 · 2016: 14 · 2015: 11 · 2014: 15 · 2013: 5
FWCI
10.95
Type
journal article
Language
en
Open access
Locations
  • Proceedings of the National Academy of Sciences (publishedVersion)
  • Europe PMC (PubMed Central) (publishedVersion)
  • PubMed Central (publishedVersion)
  • PubMed (publishedVersion)
  • MDC Repository (Max-Delbrueck-Center for Molecular Medicine) (submittedVersion)
Topics
  • Health Sciences › Medicine › Epidemiology › Autophagy in Disease and Therapy
  • Health Sciences › Medicine › Neurology › Neuroblastoma Research and Treatments
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Histone Deacetylase Inhibitors Research
Keywords
HDAC10, autophagy, neuroblastoma, chemoresistance, doxorubicin, HSP70, autophagic flux, p62/sequestosome 1, v-myc, tumor cell survival, prognostic factors
MeSH terms
Autophagy, Cell Survival, Histone Deacetylases, Humans, Neuroblastoma, Protein Binding, HSP70 Heat-Shock Proteins, Reverse Transcriptase Polymerase Chain Reaction, Cell Line, Tumor, Histone Deacetylase Inhibitors, Real-Time Polymerase Chain Reaction

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