Hsu J.-L.Leong P.-K.Ho Y.-F.LIH-CHING HSULu P.-H.Chen C.-S.JIH-HWA GUH2021-06-022021-06-0220123043835https://www.scopus.com/inward/record.uri?eid=2-s2.0-84862793343&doi=10.1016%2fj.canlet.2012.01.004&partnerID=40&md5=769176657b0879e907fc3fe18dba786ehttps://scholars.lib.ntu.edu.tw/handle/123456789/564805The knockdown of Pim-1 or inhibition of Pim-1 activity significantly increased γ-H2A.X expression. The effect was correlated to apoptosis and was attributed to the inhibition of nonhomologous DNA-end-joining (NHEJ) repair activity supported by the following observations: (1) inhibition of ATM and DNA-PKcs activities, (2) down-regulation of Ku expression and nuclear localization and (3) decrease of DNA end-binding of both Ku70 and Ku80. The data suggest that Pim-1 plays a crucial role in the regulation of NHEJ repair. In the absence of Pim-1, the ability of DNA repair significantly decreases when exposed to paclitaxel, leading to severe DNA damage and apoptosis. ? 2012 Elsevier Ireland Ltd.[SDGs]SDG3ATM protein; histone H2AX; Ku antigen; Ku80 antigen; paclitaxel; protein kinase Pim 1; small interfering RNA; unclassified drug; apoptosis; article; cell nucleus; controlled study; correlation analysis; DNA end joining repair; down regulation; gene silencing; human; human cell; male; priority journal; prostate cancer; protein expression; protein function; protein localization; Apoptosis; Cell Line, Tumor; Cell Proliferation; DNA End-Joining Repair; DNA Helicases; DNA-Binding Proteins; Drug Resistance, Neoplasm; Gene Knockdown Techniques; Histones; Humans; Male; Microtubules; Paclitaxel; Prostatic Neoplasms; Proto-Oncogene Proteins c-pim-1journal article10.1016/j.canlet.2012.01.004222613372-s2.0-84862793343