作者: Patricia L Yeyati , Rita Shaknovich , Sima Boterashvili , Jia Li , Helen J Ball
关键词: Cyclin B 、 Cyclin A2 、 Fusion protein 、 Cyclin A 、 Acute promyelocytic leukemia 、 Cyclin D 、 Cell growth 、 Biology 、 Cell cycle 、 Cancer research
摘要: The PLZF gene was identified by its fusion with the RARα locus in a therapy resistant form of acute promyelocytic leukemia (APL) associated t(11;17)(q23;q21) translocation. Here we describe as negative regulator cell cycle progression ultimately leading to growth suppression. can bind and repress cyclin A2 promoter while expression reverts suppressed phenotype myeloid cells expressing PLZF. In contrast RARα-PLZF, protein generated t(11;17)(q23;q21)-APL activates transcription allows A anchorage-deprived NIH3T3 cells. Therefore, is candidate target for inhibition may contribute suppressive properties Deregulation RARα-PLZF represent an oncogenic mechanism this chimeric aggressive clinical t(11;17)(q23;q21)-associated APL.