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
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)
Overview
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Integrity signals
Registry
Cites
Statistics
Verification
Claims the paper makes
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
The cited source says what the claim attributes to it.
In the citing paper
“MS-275 strongly inhibits Hdac1/2 over Hdac3 (ref. 19)”
From Tet2 is required to resolve inflammation by recruiting Hdac2 to specifically repress IL-6 (2015) · cites this paper as [19]
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
The self-check needs the paper’s full text.
Citations
Cites
Histone deacetylases (HDACs): characterization of the classical HDAC family
RUIJTER, A. J. M. D., GENNIP, A. H. V., CARON, H. N., KEMP, S., & KUILENBURG, A. B. P. V. (2003) · Biochemical Journal · doi:10.1042/bj20021321 · Cited by 3,114
HDAC6 is a microtubule-associated deacetylase
Hubbert, C., Guardiola, A., Shao, R., Kawaguchi, Y., Ito, A., Nixon, A., Yoshida, M., Wang, X.-F., & Yao, T.-P. (2002) · Nature · doi:10.1038/417455a · Cited by 2,403
Kischkel, F. C., Hellbardt, S., Behrmann, I., Germer, M., Pawlita, M., Krammer, P. H., & Peter, M. E. (1995) · The EMBO Journal · doi:10.1002/j.1460-2075.1995.tb00245.x · Cited by 2,184
Valproic acid defines a novel class of HDAC inhibitors inducing differentiation of transformed cells
Gottlicher, M. (2001) · The EMBO Journal · doi:10.1093/emboj/20.24.6969 · Cited by 1,887
Histone deacetylases and cancer: causes and therapies
Marks, P. A., Rifkind, R. A., Richon, V. M., Breslow, R., Miller, T., & Kelly, W. K. (2001) · Nature reviews. Cancer · doi:10.1038/35106079 · Cited by 1,866
Histone-deacetylase inhibitors: novel drugs for the treatment of cancer
Johnstone, R. W. (2002) · Nature Reviews Drug Discovery · doi:10.1038/nrd772 · Cited by 1,515
Targeting death and decoy receptors of the tumour-necrosis factor superfamily
Ashkenazi, A. (2002) · Nature Reviews Cancer · doi:10.1038/nrc821 · Cited by 1,360
HDAC6 Regulates Hsp90 Acetylation and Chaperone-Dependent Activation of Glucocorticoid Receptor
Kovacs, J. J., Murphy, P. J. M., Gaillard, S., Zhao, X., Wu, J.-T., Nicchitta, C. V., Yoshida, M., Toft, D. O., Pratt, W. B., & Yao, T.-P. (2005) · Molecular Cell · doi:10.1016/j.molcel.2005.04.021 · Cited by 1,153
Sprick, M. R., Weigand, M. A., Rieser, E., Rauch, C. T., Juo, P., Blenis, J., Krammer, P. H., & Walczak, H. (2000) · Immunity · doi:10.1016/s1074-7613(00)80211-3 · Cited by 794
Bali, P., Pranpat, M., Bradner, J., Balasis, M., Fiskus, W., Guo, F., Rocha, K., Kumaraswamy, S., Boyapalle, S., Atadja, P., et al. (2005) · Journal of Biological Chemistry · doi:10.1074/jbc.c500186200 · Cited by 755
Cited by
HDAC family: What are the cancer relevant targets?
Witt, O., Deubzer, H. E., Milde, T., & Oehme, I. (2009) · Cancer Letters · doi:10.1016/j.canlet.2008.08.016 · Cited by 1,069
Tet2 is required to resolve inflammation by recruiting Hdac2 to specifically repress IL-6
Zhang, Q., Zhao, K., Shen, Q., Han, Y., Gu, Y., Li, X., Zhao, D., Liu, Y., Wang, C., Zhang, X., et al. (2015) · Nature · doi:10.1038/nature15252 · Cited by 807
Ning, Z.-Q., Li, Z.-B., Newman, M. J., Shan, S., Wang, X.-H., Pan, D.-S., Zhang, J., Dong, M., Du, X., & Lu, X.-P. (2012) · Cancer Chemotherapy and Pharmacology · doi:10.1007/s00280-011-1766-x · Cited by 303
Entinostat for treatment of solid tumors and hematologic malignancies
Knipstein, J., & Gore, L. (2011) · Expert Opinion on Investigational Drugs · doi:10.1517/13543784.2011.613822 · Cited by 110
Acetylation of histone deacetylase 1 regulates NuRD corepressor complex activity
Yang, T., Jian, W., Luo, Y., Fu, X., Noguchi, C., Bungert, J., Huang, S., & Qiu, Y. (2012) · Journal of Biological Chemistry · doi:10.1074/jbc.m112.349704 · Cited by 35
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
- Published
- 2006-07-01
- Volume
- 66
- Issue
- 13
- Pages
- 6785-6792
- ISSN
- 0008-5472
- 1538-7445
- Cited by
- 120
- References
- 50
- Language
- en
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review
Data sources
Bibliographic data: Semantic Scholar, OpenAlex, Crossref.
Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.
