Role of Bin1 in Cellular Senescence and Apoptosis by E2F1 in Androgen-Independent Prostate Cancer Cells

Cancer is a disease of aberrant cell growth. The c-Myc oncogene is commonly activated in tumors, including prostate cancers, and its over expression has been linked to both cell cycle progression and the induction of apoptosis; however the ambiguous role of this transcription factor has yet to be elucidated. The c-Myc function lies between two signaling networks that target its C-terminal DNA binding domain as well as its N-termini transcriptional activation domain. Bin1 (Bridge integrator-1) is a Myc-interacting protein that associates with the N-terminus of the Myc oncoprotein and inhibits malignant transformation induced by c-Myc and adenovirus E1A'. However, deletion mutants of Bin1 lacking the Myc-binding domain (MBD) were still capable of inhibiting cellular transformation of oncogenic Ras mediated by adenovirus ElA, thus indicating that Bini can inhibit malignant cell growth in a Myc-independent manner.
The original document contains color images. All DTIC reproductions will be in black and white.