Lotan R, Lotan D, Meromsky L
Cancer Res. 1984 Dec;44(12 Pt 1):5805-12.
Retinoic acid inhibits the proliferation of the murine melanoma clone S91-C-2 cells, enhances the glycosylation of specific cell surface sialoglycoproteins, and stimulates sialytransferase activity. Mutant clones, selected from the S91-C-2 cells for resistance to the growth-inhibitory effect of retinoic acid, were used to explore whether cell surface modulation by retinoic acid is related to growth inhibition. Glycoprotein synthesis was assessed by analysis of [3H]glucosamine incorporation into glycoconjugates, and cell surface sialo- and galactoglycoproteins were analyzed after radiolabeling by the NaIO4:NaB3H4 and the neuraminidase plus galactose oxidase:NaB3H4 methods, respectively. The cells were solubilized and the labeled molecules were separated by polyacrylamide gel electrophoresis and identified by fluorography. Sialytransferase activity was measured in detergent-solubilized cells, using cytidine 5' -monophosphate-[14C]sialic acid as a sugar donor and asialofetuin as an exogenous acceptor. The results demonstrated that retinoic acid enhanced [3H]glucosamine incorporation into a Mr 160,000 glycoprotein in the S91-C-2 cells but not in any of the resistant mutant clones, while the pattern of [35S]methionine-labeled proteins was not modified in either the sensitive or the resistant clones. Radiolabeling of a Mr 160,000 sialoglycoprotein on the surface of S91-C-2 and of several retinoic acid-sensitive subclones of S91-C-2 was augmented by retinoic acid. A considerably smaller effect was observed on the labeling of Mr 160,000 sialoglycoprotein on one of the resistant clones, and no significant effect could be detected on the other resistant mutant clones. Sialytransferase activity was increased 2- to 3-fold by retinoic acid in the S91-C-2 cells and in several sensitive subclones, but not in any of the resistant mutant clones. Tetradecanoylphorbol acetate, which inhibits the proliferation of both retinoic acid-sensitive and retinoic acid-resistant cells, failed to increase either sialyltransferase activity or cell surface labeling of sialoglycoproteins. These findings suggest that the ability of retinoic acid to stimulate sialyltransferase activity and glycosylation of cell surface glycoproteins is related to the growth-inhibitory effect of this compound.
视黄酸可抑制小鼠黑色素瘤克隆S91-C-2细胞的增殖，增强特定细胞表面唾液酸糖蛋白的糖基化，并刺激唾液酸转移酶活性。从S91-C-2细胞中筛选出对视黄酸生长抑制作用具有抗性的突变克隆，用于探究视黄酸对细胞表面的调节是否与生长抑制有关。通过分析[3H]葡糖胺掺入糖缀合物来评估糖蛋白的合成，并分别采用高碘酸钠：硼氢化钠3H4法和神经氨酸酶加半乳糖氧化酶：硼氢化钠3H4法对细胞表面唾液酸糖蛋白和半乳糖糖蛋白进行放射性标记后进行分析。将细胞溶解，通过聚丙烯酰胺凝胶电泳分离标记分子，并通过荧光自显影进行鉴定。使用胞苷5'-单磷酸-[14C]唾液酸作为糖供体，去唾液酸胎球蛋白作为外源受体，在去污剂溶解的细胞中测量唾液酸转移酶活性。结果表明，视黄酸可增强S91-C-2细胞中[3H]葡糖胺掺入一种分子量为160,000的糖蛋白，但在任何抗性突变克隆中均未增强，而在敏感或抗性克隆中[35S]甲硫氨酸标记蛋白的模式均未改变。视黄酸增强了S91-C-2细胞表面一种分子量为160,000的唾液酸糖蛋白以及S91-C-从S91-C-2细胞中筛选出对视黄酸生长抑制作用具有抗性的突变克隆，用于探究视黄酸对细胞表面的调节是否与生长抑制有关。通过分析[3H]葡糖胺掺入糖缀合物来评估糖蛋白的合成，并分别采用高碘酸钠：硼氢化钠3H4法和神经氨酸酶加半乳糖氧化酶：硼氢化钠3H4法对细胞表面唾液酸糖蛋白和半乳糖糖蛋白进行放射性标记后进行分析。将细胞溶解使细胞溶解，通过聚丙烯酰胺凝胶电泳分离标记分子，并通过荧光自显影进行鉴定。使用胞苷5'-单磷酸-[14C]唾液酸作为糖供体，去唾液酸胎球蛋白作为外源受体，在去污剂溶解的细胞中测量唾液酸转移酶活性。结果表明，视黄酸可增强S91-C-2细胞中[3H]葡糖胺掺入一种分子量为160,000的糖蛋白，但在任何抗性突变克隆中均未增强，而在敏感或抗性克隆中[35S]甲硫氨酸标记蛋白的模式均未改变。视黄酸增强了S91-C-2细胞表面一种分子量为160,000的唾液酸糖蛋白以及S91-C-2的几个对视黄酸敏感的亚克隆的标记。在其中一个抗性克隆中观察到对视黄酸增强了S91-C-2细胞表面一种分子量为160,000的唾液酸糖蛋白以及S91-C-2的几个对视黄酸敏感的亚克隆的标记。在其中一个抗性克隆中观察到对视黄酸增强了S91-C-2细胞表面一种分子量为160,000的唾液酸糖蛋白以及S91-C-2的几个对视黄酸敏感的亚克隆的标记。在其中一个抗性克隆中观察到对分子量为160,000的唾液酸糖蛋白标记的影响要小得多，而在其他抗性突变克隆中未检测到显著影响。视黄酸使S91-C-2细胞和几个敏感亚克隆中的唾液酸转移酶活性增加2至3倍，但在任何抗性突变克隆中均未增加。十四烷酰佛波醇乙酸酯可抑制对视黄酸敏感和对视黄酸有抗性的细胞的增殖，但未能增加唾液酸转移酶活性或细胞表面唾液酸糖蛋白的标记。这些发现表明，视黄酸刺激唾液酸转移酶活性和细胞表面糖蛋白糖基化的能力与该化合物的生长抑制作用有关。 2的几个对视黄酸敏感的亚克隆的标记。在其中一个抗性克隆中观察到对分子量为160,000的唾液酸糖蛋白标记的影响要小得多，而在其他抗性突变克隆中未检测到显著影响。视黄酸使S91-C-2细胞和几个敏感亚克隆中的唾液酸转移酶活性增加2至3倍，但在任何抗性突变克隆中均未增加。十四烷酰佛波醇乙酸酯可抑制对视黄酸敏感和对视黄酸有抗性的细胞的增殖，但未能增加唾液酸转移酶活性或细胞表面唾液酸糖蛋白的标记。这些发现表明，视黄酸刺激唾液酸转移酶活性和细胞表面糖蛋白糖基化的能力与该化合物的生长抑制作用有关。
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