Stable overexpression of either mutant- or wild type SPOP in presence/absence of ΔERG in LNCaP prostate cancer cells

Purpose: Little is known about the interplay of driver mutations that never co-occur within the same cancer cells. The latter scenario has been identified in prostate cancer where recurrent gene fusions involving the oncogenic ERG transcription factor and point mutations in the ubiquitin ligase adaptor SPOP are strictly mutually exclusive. We show that ERG and mutant SPOP – even though oncogenic on their own – are together synthetic sick. Description: LNCaP cells in presence/absence of stable ΔERG overexpression, were infected with lentivirus to overexpress either wild-type or mutant SPOP (Y87C, F102C, W131G, F133S).