Prohibitin promotes apoptosis of promyelocytic leukemia induced by arsenic sulfide
作者： PENGCHENG HE , YANFENG LIU , JUN QI , HUACHAO ZHU , YUAN WANG
关键词: Promyelocytic leukemia protein 、 Prohibitin 、 Biology 、 Transfection 、 Apoptosis 、 Fusion protein 、 Arsenic sulfide 、 Acute promyelocytic leukemia 、 Cancer research 、 Arsenic trioxide
摘要: Arsenic sulfide (As4S4), an oral form of arsenic agent, has been shown to have similar efficacy and safety intravenous trioxide in the treatment acute promyelocytic leukemia (APL). The aim present study was identify proteins modulated by As4S4 determine their involvement apoptotic pathway. We used comparative proteomic analysis screen that were differentially expressed with treatment. Prohibitin (PHB) selected for its diverse role increased expression cells treated As4S4. To examine whether PHB play a functional role, two clones PHB-knockdown PHB-overexpression generated transfection NB4-R1 vectors containing gene sequences. In comparison parental cells, overexpression showed increase baseline apoptosis enhanced response As4S4-induced apoptosis. PML-RARα fusion protein found be reduced PHB-overexpression, following treatment, greater reduction leukemia-retinoic acid receptor-α (PML-RARα) seen than cells. Consistently, knockdown presented significant lesser degree degradation. results indicate antitumor activity promoting APL
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