biostudies-literatureRen SNCI NIH HHS1121-32https://www.ebi.ac.uk/biostudies/studies/S-EPMC3650856biostudies-literatureUnknown90(10)Thalidomide is experimentally used to treat various human cancers; however, clinical responses to thalidomide are sporadic. Here we demonstrate that CUL4A plays an oncogenic role in prostate cancer development and prostate cancer cells with higher level of CUL4A are particularly sensitive to thalidomide treatment. We show that CUL4A is frequently overexpressed in human primary prostate cancer and cell lines. Notably, subjects with tumors that highly expressed CUL4A had poor overall survival. CUL4A downregulation inhibited cell proliferation and induced apoptosis in vitro and in vivo, whereas CUL4A overexpression transformed human normal prostate epithelial cells and promoted invasion, which was attenuated by the extracellular signal-regulated kinase (ERK) inhibitor. We further show that thJournal of molecular medicine (Berlin, Germany)Oncogenic CUL4A determines the response to thalidomide treatment in prostate cancer.PMC3650856R01 CA116481R01 CA140654Lu XLiang YXu CWang FMao JHSun YWei MCui ZLu JGao XRen SXu WYu YfalseOncogenic CUL4A determines the response to thalidomide treatment in prostate cancer.Thalidomide is experimentally used to treat various human cancers; however, clinical responses to thalidomide are sporadic. Here we demonstrate that CUL4A plays an oncogenic role in prostate cancer development and prostate cancer cells with higher level of CUL4A are particularly sensitive to thalidomide treatment. We show that CUL4A is frequently overexpressed in human primary prostate cancer and cell lines. Notably, subjects with tumors that highly expressed CUL4A had poor overall survival. CUL4A downregulation inhibited cell proliferation and induced apoptosis in vitro and in vivo, whereas CUL4A overexpression transformed human normal prostate epithelial cells and promoted invasion, which was attenuated by the extracellular signal-regulated kinase (ERK) inhibitor. We further show that th2012-01-01T00:00:00Z2012 Oct2025-04-04T01:05:54.52Z2019-03-27T01:09:49ZS-EPMC36508562242215110.1007/s00109-012-0885-0