PubMed · 13374885
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J DUHAMEL. 1956. [The false appendicitis].. https://pubmed.ncbi.nlm.nih.gov/13374885/
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The promyelocytic leukemia zinc-finger protein (PLZF) is a transcriptional repressor. To investigate the role of PLZF in the regulation of cytoadhesion molecules involved in the mobilization of hemopoietic cells, we have analysed PLZF and very late antigen 4 (VLA-4) expression in normal and leukemic cells. In hematopoiesis, we found a negative correlation between PLZF and VLA-4 expression, except for the megakaryocytic lineage. In contrast, we observed a positive correlation between PLZF and VLA-4 expression in a panel of acute myeloid leukemia (AML) samples. In K562 cells expressing PLZF (K562-PLZF), we found that the expression of VLA-4 and c-kit was downmodulated. We have investigated the possibility for VLA-4 or the c-kit receptor to be direct target genes of PLZF in K562-PLZF cells and identified a PLZF DNA-binding site within the VLA-4 promoter. Furthermore, decrease in VLA-4 expression was associated with loss of adhesion on fibronectin-coated plates, which promotes drug-induced apoptosis of K562-PLZF cells. Our findings indicate that VLA-4 is a potential target gene of PLZF. However, in primary AMLs the control of PLZF on VLA-4 expression is lost. Altogether, we suggest that VLA-4 modulation by PLZF may represent an important step in the control of normal and leukemic cell mobilization.
We reported previously that KG-1, a human acute leukemia cell line, has mutational loss of 8-oxoguanine (8-hydroxyguanine; oh8Gua) glycosylase 1 (OGG1) activity and undergoes apoptotic death after treatment with 7,8-dihydro-8-oxo-2'-deoxyguanosine (8-oxodeoxyguanosine, 8-hydroxydeoxyguanosine; oh8dG). In our present study, we further characterized the effects of oh8dG in KG-1 cells and found that, in addition to apoptosis, oh8dG induced the arrest of KG-1 at the G1 phase. Simultaneously, oh8dG-treated KG-1 showed an increase in the oh8Gua content of DNA, upregulation of p21 (an inhibitor of cdk), and Ras inactivation. Moreover, the upregulation of p21 was followed by the inactivations of cdk4 and cdk2, the hypophosphorylation of Rb, and a marked decline in the expression of c-myc (a gene regulated by E2F that is a transcription factor whose activity is suppressed when it is bound to hypophosphorylated Rb). Ras inactivation was also followed by the inactivation of ERK kinase (MEK) and the inactivation of AP-1, a downstream target of the Ras signaling pathway. The specific MEK inhibitors, PD98059 and U0126, also induced G1 arrest. These findings suggest that p21 upregulation and Ras inactivation contribute to G1 arrest. An increase of oh8Gua content in DNA does not seem to be a principal contributor to G1 arrest, however, because the kinetics of increases of oh8Gua content in DNA and of G1 cell number did not coincide. We report that oh8dG induces the arrest of KG-1 growth at the G1 phase mainly by upregulating p21 and inactivating Ras.
We describe a patient who presented myoclonus in the left scapula 3 months after a traumatic lesion of the left long thoracic nerve. Myoclonic activity was recorded as pseudorhythmic electromyographic bursts repeated at a frequency of 2 to 4 Hz, each lasting between 100 and 200 msec, in the left serratus-dorsalis muscle region, trapezius, and deltoid muscles. A combination of peripheral and central mechanisms may have induced the myoclonus in this case.