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胰岛素或乏血小板血浆对c-myc信使核糖核酸水平的调控

Regulation of c-myc mRNA levels by insulin or platelet-poor plasma.

作者信息

Gai X X, Rizzo M G, Valpreda S, Baserga R

机构信息

Department of Pathology, Temple University Medical School, Philadelphia, Pennsylvania 19140.

出版信息

Oncogene Res. 1989;5(2):111-20.

PMID:2691956
Abstract

Cell lines have been permanently established from BALB/c3T3 cells that constitutively express either the murine p53, the human IGF-1 gene, or both (Gai et al., 1988). The derivative cell lines grow well in platelet-poor plasma or in serum-free medium supplemented with the appropriate growth factors, while BALB/c3T3 cells do not grow in platelet-poor plasma, nor do they grow in serum-free medium unless supplemented with both platelet-derived growth factor and insulin (or IGF-1). In BALB/c3T3 cells, steady-state levels of c-myc mRNA decrease promptly and sharply once the cells are transferred to platelet-poor plasma. In the derivative cell lines, constitutively expressing p53, IGF-1, or both, c-myc mRNA levels remain elevated and actually increase when the cells are transferred to platelet-poor plasma. In serum-free medium, the c-myc mRNA levels decreased in BALB/c3T3 cells, as well as in the derivative cell lines. However, in the latter cell lines, but not in BALB/c3T3, the addition of platelet-poor plasma or insulin again increased the expression of c-myc. The increase in c-myc mRNA levels could be partially explained by an increase in transcription. These results indicate that in certain cell lines the expression of c-myc mRNA can be induced by insulin or platelet-poor plasma.

摘要

已从组成型表达鼠p53、人IGF-1基因或两者的BALB/c3T3细胞中永久建立了细胞系(Gai等人,1988年)。衍生细胞系在贫血小板血浆或补充了适当生长因子的无血清培养基中生长良好,而BALB/c3T3细胞在贫血小板血浆中不生长,在无血清培养基中也不生长,除非同时补充血小板衍生生长因子和胰岛素(或IGF-1)。在BALB/c3T3细胞中,一旦细胞转移到贫血小板血浆中,c-myc mRNA的稳态水平会迅速且急剧下降。在组成型表达p53、IGF-1或两者的衍生细胞系中,当细胞转移到贫血小板血浆中时,c-myc mRNA水平保持升高,实际上还会增加。在无血清培养基中,BALB/c3T3细胞以及衍生细胞系中的c-myc mRNA水平均下降。然而,在后者细胞系中,而非BALB/c3T3细胞中,添加贫血小板血浆或胰岛素会再次增加c-myc的表达。c-myc mRNA水平的增加部分可由转录增加来解释。这些结果表明,在某些细胞系中,c-myc mRNA的表达可被胰岛素或贫血小板血浆诱导。

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