Gupta Pallavi, Gurudutta Gangenahalli U, Verma Yogesh K, Kishore Vimal, Gulati Shweta, Sharma R K, Chandra Ramesh, Saluja Daman
Stem Cell Gene Therapy Research Group, Institute of Nuclear Medicine & Allied Sciences (INMAS), DRDO, Delhi-110054, India.
Stem Cells Dev. 2006 Aug;15(4):609-17. doi: 10.1089/scd.2006.15.609.
The hematopoietic transcription factor PU.1, which is required for lymphomyeloid differentiation of stem cells, was originally identified as an oncogene. In erythroid progenitors, the integration of spleen focus-forming virus (SFFV) into the PU.1 locus causes its overexpression, which blocks their terminal differentiation into erythrocytes and ultimately leads to the development of erythroleukemia. However, in myeloid lineages, PU.1 promotes granulocytic and monocytic differentiation, and graded reduction in its expression blocks their differentiation or maturation and thereby causes myelogenous leukemia. Thus, in addition to normal hematopoietic regulation, PU.1 plays a significant role in leukemogenesis. In the following review, we have consolidated our understanding of the role of transcription factor PU.1 in the development of erythroid as well myeloid leukemia.
造血转录因子PU.1是干细胞淋巴髓系分化所必需的,最初被鉴定为一种癌基因。在红系祖细胞中,脾集落形成病毒(SFFV)整合到PU.1基因座会导致其过度表达,这会阻止它们终末分化为红细胞,并最终导致红白血病的发生。然而,在髓系谱系中,PU.1促进粒细胞和单核细胞分化,其表达的分级降低会阻止它们的分化或成熟,从而导致髓性白血病。因此,除了正常的造血调节外,PU.1在白血病发生中也起着重要作用。在以下综述中,我们巩固了对转录因子PU.1在红系和髓系白血病发展中作用的理解。