Abstract
The adenovirus-5 E1A gene encodes two main proteins of 289 and 243 amino acid residues from 13S and 12S mRNA, respectively. The E1A gene products function as transcriptional regulators and have anti-tumor activities. Despite the fact that E1A gene therapy has been tested in clinical trials, the molecular mechanism by which it suppresses tumor cell growth is still not completely understood. Here, we show that E1A increases the expression of the cyclin-dependent kinase (CDK) inhibitor p21 WAF1/CIP1, which inhibits cell growth. We further show that 13S E1A, but not 12S E1A, can transactivate the p21 promoter through Sp1 sites. Interestingly, the E1A-induced transactivation occurs only in cancer cells, not in normal cells. This study provides new insight into the links between E1A and the CDK inhibitor and may have important clinical implications.
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
More From: Biochemical and Biophysical Research Communications
Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.