Retinoblastoma tumor suppressor status is a critical determinant of therapeutic response in prostate cancer cells.

ABSTRACT: The retinoblastoma tumor suppressor protein (RB), a critical mediator of cell cycle progression, is functionally inactivated in the majority of human cancers, including prostatic adenocarcinoma. The importance of RB tumor suppressor function in this disease is evident because 25% to 50% of prostatic adenocarcinomas harbor aberrations in RB pathway. However, no previous studies challenged the consequence of RB inactivation on tumor cell proliferation or therapeutic response. Here, we show that RB depletion facilitates deregulation of specific E2F target genes, but does not confer a significant proliferative advantage in the presence of androgen. However, RB-deficient cells failed to elicit a cytostatic response (compared with RB proficient isogenic controls) when challenged with androgen ab

SUBMITTER: Sharma A 

PROVIDER: S-EPMC4133940 | biostudies-literature | 2007 Jul

REPOSITORIES: biostudies-literature