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PMID: 16123597 Published · ppublish English Journal Article

DeltaNp63alpha levels correlate with clinical tumor response to cisplatin.

Cell cycle (Georgetown, Tex.) ·Vol. 4 ·No. 10 ·2005-10-00 ·Pages 1313-5

Zangen R, Ratovitski E, Sidransky D

Abstract

After exposure to damaging agents, the p53 tumor suppressor is stabilized mediating cell cycle arrest and apoptosis. p53 family member, DeltaNp63 promotes cell proliferation and accelerates tumor growth. We previously found that the genotoxic stress agents induced a decrease of DeltaNp63alpha. We further observed that genotoxic stress mediated phosphorylation of DeltaNp63alpha targeting it into proteasome degradation. Here, we found that high DeltaNp63 protein levels in primary tumors accurately predicted response to platinum based chemotherapy and a favorable outcome in head and neck cancer patients. Our data suggest that degradation of DeltaNp63alpha is part of the cellular response to DNA damage in head and neck cancers. The findings may have implications for the rational use of DNA damaging agents in human cancer.

MeSH Terms
Animals Cisplatin/pharmacology,therapeutic use Gene Expression Regulation Humans Neoplasms/drug therapy,genetics,metabolism,pathology Protein Subunits/genetics,metabolism Tumor Suppressor Proteins/genetics,metabolism
Chemicals
Protein Subunits Tumor Suppressor Proteins Cisplatin
Authors & Affiliations
3 authors, click to expand affiliations / ORCID
Zangen Rachel
Department of Otolaryngology/Head and Neck Surgery, The Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA.
Ratovitski Edward
Sidransky David
Article Info
Journal
Cell cycle (Georgetown, Tex.)
Abbr.
Cell Cycle
ISSN
1551-4005
Published
2005-10-00
Epub
2005-00-01
Pages
1313-5
Language
English
Region
United States
NLM ID
101137841
Subset
IM
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