Requirement for ERK Activity in Sodium Selenite-induced Apoptosis of Acute Promyelocytic Leukemia-derived NB4 Cells

Received 2 April 2006, Accepted 17 October 2006Our previous study has shown that sodium selenite cancause apoptosis in acute promyelocytic leukemia-derivedNB4 cells in a caspase-dependent manner, but the detailedmechanism unkis nown H. e were demonstrae taequir r ementfor extracellular signal-regulated protein kinase (ERK) inmediating sodium selenite -induced apoptosis in NB4 cell.Though no apparent elevation of ERK activity was observedduring the apoptosis in NB4 cells caused by2 0 µ M sodiumselenite treatment, PD98059 and U0126, specific chemicalinhibitors o tfhe MEK/ERK gnis aling pathw wer, aye shownto strongly prevent the apoptosis process, while ERKactivator TPA enhanced the process. It is also known thatSP600125M APK inhibip38 SB2r 03580 and JNtoronhibit K ihad slight effects on apoptosis. Further study indicatedthat ERK exerted its proapoptotic effect only at the earlystage of apoptosis and played an antiapoptotic role at thelater stages. Taken together, our findings suggest thatERK plays an active role in mediating sodium selenite-induced apoptosis in NB4 cells .Keyword: s Acute promyelocytic leukemia-derived NB4 cells,Apoptosis, ERK Activity, MEK Inhibitior, Sodium Selenite