In hypoxia-stressed prostate cancer cells of two other cell lines (LNCaP and C4-2B), overexpressed HIF-1α was shown to ensure the enhanced β-catenin nuclear translocation that led to radioresistance due to an altered cell cycle, reduced apoptotic death and improved nonhomologous end joining in the post-radiation DNA break repair [45]. Here, HIF1A is linked to prostate carcinoma.