Lotan R, Lotan D, Amos B
Department of Tumor Biology, University of Texas, M. D. Anderson Hospital and Tumor Institute, Houston 77030.
Exp Cell Res. 1988 Aug;177(2):284-94. doi: 10.1016/0014-4827(88)90462-4.
Previous studies have demonstrated the ability of retinoic acid (RA) to inhibit the growth of two spontaneous murine melanoma cell lines (B16-F1 and S91-C2) and to augment both sialyltransferase activity and the sialylation of an Mr 160,000 cell-surface glycoprotein. The present study examined the effects of RA on an ultraviolet irradiation-induced murine melanoma cell line K-1735P. Like the two spontaneous melanomas, the uv-induced melanoma exhibited susceptibility to the growth-inhibitory action of RA. Both the anchorage-dependent and the anchorage-independent growths of the K-1735P cells were suppressed by RA, with IC50 values of 5 X 10(-9) and 3 X 10(-12) M, respectively. Sialyltransferase activity in both S91-C2 and K-1735P cells treated with 10(-6) or 10(-5) M RA increased two- and three-fold, respectively, as compared with untreated cells. In contrast, cell-surface sialo- and galactoglycoproteins, revealed by labeling with periodate and tritiated borohydrate or with neuraminidase, galactose oxidase, and tritiated borohydrate, respectively, varied between the S91-C2 and the K-1735P cells, and each cell line's modulation by RA was also distinct. These findings suggest that although RA can increase the activity of sialyltransferase in different melanoma cells, this increased activity may, in turn, result in an increased sialylation of distinct cell-surface glycoproteins.
先前的研究已证明视黄酸(RA)能够抑制两种自发性小鼠黑色素瘤细胞系(B16-F1和S91-C2)的生长,并增强唾液酸转移酶活性以及一种分子量为160,000的细胞表面糖蛋白的唾液酸化。本研究检测了RA对紫外线照射诱导的小鼠黑色素瘤细胞系K-1735P的影响。与两种自发性黑色素瘤一样,紫外线诱导的黑色素瘤对RA的生长抑制作用敏感。RA抑制了K-1735P细胞的贴壁依赖性生长和非贴壁依赖性生长,其IC50值分别为5×10^(-9) M和3×10^(-12) M。用10^(-6)或10^(-5) M RA处理的S91-C2和K-1735P细胞中的唾液酸转移酶活性,与未处理的细胞相比,分别增加了两倍和三倍。相比之下,通过高碘酸盐和氚化硼氢化钠标记或分别用神经氨酸酶、半乳糖氧化酶和氚化硼氢化钠标记所显示的细胞表面唾液酸糖蛋白和半乳糖糖蛋白,在S91-C2和K-1735P细胞之间有所不同,并且每种细胞系受RA的调节也不同。这些发现表明,尽管RA可以增加不同黑色素瘤细胞中唾液酸转移酶的活性,但这种增加的活性反过来可能导致不同细胞表面糖蛋白的唾液酸化增加。