Alterations of MCF-7 human breast cancer cell after prostaglandins PGA1 and PGF2 alpha treatment.

Experimental cell biology Pub Date : 1987-01-01
N A Shahabi, N Chegini, J L Wittliff
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引用次数: 0

Abstract

Treatment of monolayer cultures of MCF-7 cells with prostaglandins PGA1 and PGF2 alpha inhibited cell proliferation, reduced the rate of labeled precursor incorporation into DNA, RNA, and protein, and induced morphological changes in a dose-dependent manner. The rate of [3H]thymidine incorporation was increased by PGA1 at 10(-10)-10(-8) M, while a sharp decrease was observed at 10(-6)-10(-4) M (p less than 0.05 and p less than 0.005). PGF2 alpha inhibited [3H]thymidine incorporation at all concentrations tested. Similar results were obtained for [3H]uridine incorporation with both PGs. PGA1 inhibited [3H]leucine incorporation at 10(-4) M, but increased incorporation at 10(-10)-10(-6) M. At the ultrastructural level, neither PG induced morphological alterations at 10(-12)-10(-8) M. However, at 10(-6)-10(-4) M both PGA1 and PGF2 alpha diminished the number and size of cell surface projections; some cells appeared to completely lack microvilli. Disorganization of mitochondrial cristae and increased electron density of the matrix were also evident.

前列腺素PGA1和PGF2 α治疗后MCF-7人乳腺癌细胞的变化
用前列腺素PGA1和PGF2 α处理MCF-7细胞单层培养物可抑制细胞增殖,降低标记前体掺入DNA、RNA和蛋白质的速率,并以剂量依赖性方式诱导形态学改变。PGA1在10(-10)-10(-8)M时使[3H]胸苷的掺入率增加,而在10(-6)-10(-4)M时使[3H]胸苷的掺入率急剧下降(p < 0.05和p < 0.005)。在所有测试浓度下,PGF2抑制[3H]胸苷结合。[3H]尿苷与两种pg的掺入结果相似。PGA1在10(-4)M时抑制[3H]亮氨酸的掺入,但在10(-10)-10(-6)M时增加掺入。在超微结构水平上,PG在10(-12)-10(-8)M时均未引起形态学改变。然而,在10(-6)-10(-4)M时,PGA1和PGF2 α均减少了细胞表面突起的数量和大小;有些细胞似乎完全没有微绒毛。线粒体嵴解体,基质电子密度增加。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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