Fig. 4

Upregulation of ATM by N-Myc contributes to Enzalutamide resistance of C4–2 cells. a Immunohistochemistry staining of N-Myc, ATM and phospho-ATM at serine 1981 (p-ATMS1981) in human benign prostate, adenocarcinoma prostate cancer (AdCa), CRPC and NEPC tissues. b-d Quantification of N-Myc, ATM and p-ATMS1981 IHC staining from (a). e Cell viability of different C4–2 cells treated with 10 μM Enzalutamide over a time course. C4–2/Ctrl and C4–2/ATM−/− represents CRISPR control and CRISPR ATM knockout while C4–2/Ctrl/N-Myc and C4–2/ATM−/−/N-Myc are the cells with N-Myc overexpression introduced by lentivirus infection. f Dose response of ATM inhibitor Ku60019 at 72 h using MTS cell viability assay for C4–2/Vec and C4–2/N-Myc cells. g Cell viability of C4–2/N-Myc treated with DMSO, Enzalutamide (10 μM), ATMi Ku60019 (2 μM) and in combination (Enza (10 μM) + ATMi (2 μM)) over a time course. *p < 0.05, **p < 0.005