Document Detail


PS-341 and histone deacetylase inhibitor synergistically induce apoptosis in head and neck squamous cell carcinoma cells.
MedLine Citation:
PMID:  20571067     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Proteasome inhibitor PS-341 (also known as bortezomib) and histone deacetylase (HDAC) inhibitors have emerged as novel therapeutic agents for a variety of malignancies. In this study, we examined whether PS-341 and the HDAC inhibitor trichostatin A (TSA) induced apoptosis in head and neck squamous cell carcinoma (HNSCC), a common and lethal malignancy. We found that, although TSA treatment alone did not induce apoptosis in HNSCC cells, it significantly enhanced PS-341-induced apoptosis in HNSCC cells in vitro. Consistently, TSA significantly improved PS-341-mediated inhibition of HNSCC tumor growth in nude mice. Mechanistically, we found that TSA increased PS-341-induced Noxa expression and caspase activation in HNSCC cells. The knockdown of Noxa significantly reduced apoptosis induced by cotreatment of PS-341 and TSA. Taken together, our results provide new insight into the mechanisms of synergistic antitumor activity of the PS-341 and HDAC inhibitor regimen, offering a new therapeutic strategy for HNSCC patients.
Authors:
Jinkoo Kim; Jean Guan; Insoon Chang; Xiaohong Chen; Demin Han; Cun-Yu Wang
Related Documents :
15084347 - Screening of some anti-androgenic endocrine disruptors using a recombinant cell-based i...
20454597 - Human copper transporters: mechanism, role in human diseases and therapeutic potential.
20429927 - The chemotherapeutic agent bortezomib induces the formation of stress granules.
9713497 - Clonal variability of radiation-induced cisplatin resistant hela cells.
1502427 - The neuro-immune network. some recent developments.
10899937 - The neuronal microtubule-associated protein tau is a substrate for caspase-3 and an eff...
Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural     Date:  2010-06-22
Journal Detail:
Title:  Molecular cancer therapeutics     Volume:  9     ISSN:  1538-8514     ISO Abbreviation:  Mol. Cancer Ther.     Publication Date:  2010 Jul 
Date Detail:
Created Date:  2010-07-09     Completed Date:  2010-11-04     Revised Date:  2011-08-01    
Medline Journal Info:
Nlm Unique ID:  101132535     Medline TA:  Mol Cancer Ther     Country:  United States    
Other Details:
Languages:  eng     Pagination:  1977-84     Citation Subset:  IM    
Copyright Information:
(c)2010 AACR.
Affiliation:
Division of Oral Biology and Medicine, School of Dentistry, University of California, Los Angeles, Los Angeles, California 90095, USA.
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Descriptor/Qualifier:
Acetylation / drug effects
Animals
Antineoplastic Agents / administration & dosage,  pharmacology
Antineoplastic Combined Chemotherapy Protocols / therapeutic use
Apoptosis / drug effects*
Blotting, Northern
Blotting, Western
Boronic Acids / administration & dosage,  pharmacology*
Carcinoma, Squamous Cell / drug therapy*,  metabolism,  pathology
Caspases / metabolism
Cell Line, Tumor
Dose-Response Relationship, Drug
Drug Synergism
Enzyme Activation / drug effects
Head and Neck Neoplasms / drug therapy*,  metabolism,  pathology
Histone Deacetylase Inhibitors / administration & dosage,  pharmacology
Histones / metabolism
Humans
Hydroxamic Acids / administration & dosage,  pharmacology*
Mice
Mice, Nude
Proto-Oncogene Proteins c-bcl-2 / genetics,  metabolism
Pyrazines / administration & dosage,  pharmacology*
RNA Interference
Xenograft Model Antitumor Assays
Grant Support
ID/Acronym/Agency:
DE13848/DE/NIDCR NIH HHS; DE15964/DE/NIDCR NIH HHS; R01 DE015964-08/DE/NIDCR NIH HHS; R37 DE013848-11/DE/NIDCR NIH HHS
Chemical
Reg. No./Substance:
0/Antineoplastic Agents; 0/Boronic Acids; 0/Histone Deacetylase Inhibitors; 0/Histones; 0/Hydroxamic Acids; 0/PMAIP1 protein, human; 0/Proto-Oncogene Proteins c-bcl-2; 0/Pyrazines; 0/bortezomib; 58880-19-6/trichostatin A; EC 3.4.22.-/Caspases
Comments/Corrections

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


Previous Document:  Telomerase as an important target of androgen signaling blockade for prostate cancer treatment.
Next Document:  The Dynamin Inhibitors MiTMAB and OcTMAB Induce Cytokinesis Failure and Inhibit Cell Proliferation i...