PLK1 is a crucial downstream effector of PDK1 for MYC activation and cell survival. PLK1 is a crucial downstream effector of PDK1 for MYC activation and.

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Presentation transcript:

PLK1 is a crucial downstream effector of PDK1 for MYC activation and cell survival. PLK1 is a crucial downstream effector of PDK1 for MYC activation and cell survival. A, cell viability of HEK-vector, HEK-PDK1, and HEK-E545K cells treated with the indicated concentrations of BI2536 and GW843682X for 4 days. B, cell viability of RWPE-1 and HMEC-derived cell lines treated with 10 nmol/L BI2536 for 4 days. C, immunoblot analysis of PLK1 in indicated cell lines. D, soft-agar growth of indicated cell lines treated with 10 nmol/L BI2536 for 14 days. E, immunoblot analysis in HEK-PDK1 and -MYC cells treated with BI2536 and GW843682X at indicated concentration for 24 hours. F, apoptosis by sub-G1 analysis of indicated cell lines treated with 10 nmol/L BI2536 for 48 hours. G, apoptosis of indicated cell lines treated with NC or PLK1 siRNAs for 48 hours (top) and immunoblot analysis of indicated proteins (bottom). H, xenograft tumor growth of HEK-PDK1 and HEK-E545K cells in nude mice treated with 50 mg/kg BI2536 twice per week as described in Methods. Data are mean ± SEM (n = 5 for each group). I, cell viability assay showing the dose response of a panel of breast cancer cell lines that are MYC-dependent (MDA-MB-231, SUM159PT, and Hs578T) and -independent (T47D, BT474, MCF-10A, and HMEC) to BI2536 treatment. Jing Tan et al. Cancer Discovery 2013;3:1156-1171 ©2013 by American Association for Cancer Research