Abstract
ELL2 is a potential tumor suppressor in prostate cancer. ELL2 knockout in mice induced mPIN, the putative precursor of prostate cancer and ELL2 knockdown enhanced proliferation in cultured prostate cancer cells. To explore the mechanism of ELL2 action in prostate cancer, we investigated the role of Birc3, an apoptosis inhibitor, in prostate cancer cells and the regulation of its expression by ELL2. ELL2 knockdown enhanced Birc3 expression in LNCaP and C4-2 cell line models. BrdU assay showed that Birc3 knockdown inhibited proliferation, ELL2 knockdown enhanced proliferation, and Birc3 knockdown counteracted ELL2 knockdown-induced proliferation in LNCaP cells. Trypan blue assay suggested that Birc3 knockout did not induce cell death in LNCaP cells. These findings suggested that Birc3 is a downstream gene of ELL2 and may play a role in driving prostate cancer proliferation.