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Cited by 120

The DOI matches its Crossref record; 50 of the 50 references it cites were found in a registry or an index.

Inhibition of Histone Deacetylase Class I but not Class II Is Critical for the Sensitization of Leukemic Cells to Tumor Necrosis Factor–Related Apoptosis-Inducing Ligand–Induced Apoptosis

Inoue, Satoshi, Mai, Antonello, Dyer, Martin J.S., Cohen, Gerald M.·2006·Cancer Research
DOI 10.1158/0008-5472.can-05-4563
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Abstract

From work done largely on derived cell lines, it has been suggested that tumor necrosis factor–related apoptosis-inducing ligand (TRAIL) might be a therapeutic target for many forms of malignancy. However, use of primary tumor cells, including chronic lymphocytic leukemic (CLL) cells, has shown inherent resistance to TRAIL. Although the molecular basis for this resistance remains unknown, treatment with histone deacetylase inhibitors (HDACi) often sensitizes resistant cells to TRAIL-induced apoptosis. We used structurally diverse HDACi to ascertain which HDAC needs to be inhibited for the sensitization. Inhibition of HDAC class I but not class II is required for sensitization to TRAIL-induced apoptosis of CLL cells and various cell lines. Using different HDACi together with small interfering RNA for HDAC1, HDAC2, HDAC3, and HDAC6, we report that inhibition of HDAC1 and HDAC2 but not HDAC3, HDAC6, and HDAC8 are primarily responsible for sensitization to TRAIL-induced apoptosis. Based on these data and our previous studies, we propose that a clinical trial in CLL is warranted using a combination of a selective HDACi that inhibits HDAC1 and/or HDAC2 together with a form of TRAIL that signals through TRAIL receptor 1. (Cancer Res 2006; 66(13): 6785-92)

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Metadata

Authors
Inoue, S., Mai, A., Dyer, M. J. S., & Cohen, G. M.
Affiliations
  • 1Medical Research Council Toxicology Unit, University of Leicester, Leicester, United Kingdom; and
  • 2Istituto Pasteur, Fondazione Cenci-Bolognetti, Dipartimento di Studi Farmaceutici, Universita degli Studi di Roma “La Sapienza,” Rome, Italy
Venue
Cancer Research
Publisher
American Association for Cancer Research (AACR)
Published
2006-07-01
Volume
66
Issue
13
Pages
6785-6792
ISSN
  • 0008-5472
  • 1538-7445
DOI
10.1158/0008-5472.can-05-4563
Cited by
120
References
50
Language
en

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