Journal
CANCER CELL
Volume 9, Issue 1, Pages 45-56Publisher
CELL PRESS
DOI: 10.1016/j.ccr.2005.12.013
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Funding
- NATIONAL INSTITUTE OF DENTAL & CRANIOFACIAL RESEARCH [R01DE015945] Funding Source: NIH RePORTER
- NIDCR NIH HHS [R01 DE015945, R01 DE15945] Funding Source: Medline
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We demonstrate that Delta Np63 alpha is an essential survival factor in head and neck squamous cell carcinoma (HNSCC) through its ability to suppress p73-dependent apoptosis. Inhibition of endogenous p63 expression by RNAi induces apoptosis selectively in HNSCC cells that overexpress Delta Np63 alpha. Knockdown of p63 induces the proapoptotic bcl-2 family members Puma and Noxa, and both their induction and subsequent cell death are p53 independent but require transactivating isoforms of p73. Inhibition of p73-dependent transcription by Delta Np63 alpha involves both direct promoter binding and physical interaction with p73. In HNSCC cells lacking endogenous Delta Np63 alpha expression, bc1-2 is instead upregulated and can suppress p73-mediated death. Together, these data define a pathway whereby Delta Np63 alpha promotes survival in squamous epithelial malignancy by repressing a p73-dependent proapoptotic transcriptional program.
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