Authors: 7 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA; eng 2-s2.0-0036040930
Journal: Italy||Italy||Italy||Italy||Italy||Italy||Italy||Italy||Italy||Italy||Italy||Italy||Italy
Published: false
Volume: Corallini A.; Sampaolesi R.; Possati L.; Merlin M.; Bagnarelli P.; Piola C.; Fabris M.; Menegatti M.A.; Talevi S.; Gibellini D.; Rocchetti R.; Caputo A.; Barbanti-Brodano G., Issue: 2002, Pages: Corallini||Sampaolesi||Possati||Merlin||Bagnarelli||Piola||Fabris||Menegatti||Talevi||Gibellini||Rocchetti||Caputo||Barbanti-Brodano-The Tat protein of the human immunodeficiency virus type 1 promotes survival and growth and inhibits apoptosis of different cell types. These effects of Tat are attributed to the induction of bcl-2 gene expression. In this study we show that the blocking of both intracellular and extracellular Tat correlates with a decrease of bcl-2 transcripts, leading in vitro to a lower growth rate and attenuation of the transformed phenotype and in vivo to a reduced angiogenic and oncogenic activity of Tat-expressing cells. These results support the notion that bcl-2 is an effector of Tat-induced angiogenesis and oncogenesis and indicate that the blocking of Tat functions by immunoprophylactic, pharmacological, and gene therapy approaches may help to control oncogenesis during AIDS. © 2002 Elsevier Science (USA).