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癌基因v-fms介导的转化:栗精胺对转化相关参数的影响。

Transformation by the oncogene v-fms: the effects of castanospermine on transformation-related parameters.

作者信息

Nichols E J, Manger R, Hakomori S I, Rohrschneider L R

机构信息

Fred Hutchinson Cancer Research Center, Division of Basic Sciences, Seattle, Washington 98104.

出版信息

Exp Cell Res. 1987 Dec;173(2):486-95. doi: 10.1016/0014-4827(87)90288-6.

Abstract

The effects of castanospermine on various parameters associated with transformation were examined in cells expressing the viral oncogene v-fms. Fischer rat embryo (FRE) cells transformed by the oncogene v-fms and grown in the presence of castanospermine reverted to a more normal cell morphology and accumulated fms protein within the endoplasmic reticulum. Treated cells attained contact inhibition of cell growth at a much lower cell density compared to the untreated controls. No effect of castanospermine on cell growth was observed for FRE cells transformed by a different oncogene v-fgr. Castanospermine-treated SM-FRE (v-fms transformed) cells reexpressed extracellular matrix fibronectin and exhibited an extensive actin-containing cytoskeleton similar to that of normal nontransformed FRE cells. Castanospermine treatment of SM-FRE cells resulted in a sixfold decrease in [3H]deoxyglucose uptake compared to that of the nonreverted SM-FRE cells. Again, no effect was observed in FRE cells transformed by the oncogene v-fgr (GR-FRE). These results further characterize the reversion caused by castanospermine and indicate that cell surface expression coordinately controls anchorage independent growth, cell morphology, contact inhibition of growth, and hexose uptake.

摘要

在表达病毒癌基因v-fms的细胞中,研究了栗精胺对与转化相关的各种参数的影响。由癌基因v-fms转化并在栗精胺存在下生长的Fischer大鼠胚胎(FRE)细胞恢复到更正常的细胞形态,并在内质网中积累fms蛋白。与未处理的对照相比,处理后的细胞在低得多的细胞密度下达到细胞生长的接触抑制。对于由不同癌基因v-fgr转化的FRE细胞,未观察到栗精胺对细胞生长的影响。经栗精胺处理的SM-FRE(v-fms转化)细胞重新表达细胞外基质纤连蛋白,并表现出与正常未转化FRE细胞相似的广泛的含肌动蛋白的细胞骨架。与未回复的SM-FRE细胞相比,栗精胺处理SM-FRE细胞导致[3H]脱氧葡萄糖摄取减少六倍。同样,在由癌基因v-fgr(GR-FRE)转化的FRE细胞中未观察到影响。这些结果进一步表征了栗精胺引起的回复,并表明细胞表面表达协同控制锚定非依赖性生长、细胞形态、生长的接触抑制和己糖摄取。

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