Kozopas K M, Yang T, Buchan H L, Zhou P, Craig R W
Department of Physiology, Johns Hopkins University School of Medicine, Baltimore, MD 21205.
Proc Natl Acad Sci U S A. 1993 Apr 15;90(8):3516-20. doi: 10.1073/pnas.90.8.3516.
During their lifespan, immature cells normally pass through sequential transitions to a differentiated state and eventually undergo cell death. This progression is aberrant in cancer, although the transition to differentiation can be reestablished in inducible leukemia cell lines. This report describes a gene, MCL1, that we isolated from the ML-1 human myeloid leukemia cell line during phorbol ester-induced differentiation along the monocyte/macrophage pathway. Our results demonstrate that expression of MCL1 increases early in the induction, or "programming," of differentiation in ML-1 (at 1-3 hr), before the appearance of differentiation markers and mature morphology (at 1-3 days). They further show that MCL1 has sequence similarity to BCL2, a gene involved in normal lymphoid development and in lymphomas with the t(14;18) chromosome translocation. MCL1 and BCL2 do not fall into previously known gene families. BCL2 differs from many oncogenes in that it inhibits programmed cell death, promoting viability rather than proliferation; this parallels the association of MCL1 with the programming of differentiation and concomitant maintenance of viability but not proliferation. Thus, in contrast to proliferation-associated genes, expression of MCL1 and BCL2 relates to the programming of differentiation and cell viability/death. The discovery of MCL1 broadens our perspective on an emerging MCL1/BCL2 gene family and will allow further comparison with oncogene families.
在其生命周期中,未成熟细胞通常会经历一系列转变,进入分化状态,最终发生细胞死亡。在癌症中,这种进程是异常的,不过在可诱导的白血病细胞系中,向分化的转变可以重新建立。本报告描述了一个基因——MCL1,我们在佛波酯诱导ML-1人髓系白血病细胞系沿单核细胞/巨噬细胞途径分化的过程中,从该细胞系中分离出了这个基因。我们的结果表明,在ML-1细胞分化的诱导期或“编程”早期(1 - 3小时),即在分化标志物和成熟形态出现之前(1 - 3天),MCL1的表达就会增加。结果还进一步表明,MCL1与BCL2具有序列相似性,BCL2是一个参与正常淋巴细胞发育以及与t(14;18)染色体易位相关淋巴瘤的基因。MCL1和BCL2并不属于先前已知的基因家族。BCL2与许多癌基因不同,它抑制程序性细胞死亡,促进细胞存活而非增殖;这与MCL1在分化编程以及伴随的存活维持而非增殖中的作用相似。因此,与增殖相关基因不同,MCL1和BCL2的表达与分化编程以及细胞存活/死亡相关。MCL1的发现拓宽了我们对新兴的MCL1/BCL2基因家族的认识,并将有助于与癌基因家族进行进一步比较。