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半乳糖基转移酶活性与细胞生长:尿苷二磷酸(UDP)半乳糖对小鼠白血病L1210细胞的抑制作用

Galactosyltransferase activity and cell growth: uridine diphosphate (UDP)galactose inhibition of murine leukemic L1210 cells.

作者信息

Klohs W D, Wilson J R, Weiser M M, Frankfurt O, Bernacki R J

出版信息

J Cell Physiol. 1984 Apr;119(1):23-8. doi: 10.1002/jcp.1041190105.

DOI:10.1002/jcp.1041190105
PMID:6423650
Abstract

UDPgalactose inhibits the growth of mouse leukemic L1210 cells. In calf serum supplemented Dulbecco's medium (CS-DMEM), 1.2 mM UDPgalactose (UDPgal) inhibited cell growth by 50% (IC50), and 5 mM UDPgalactose inhibited cell growth by 92%. Other nucleotide sugars as well as galactose, glucose, and galactose-1-phosphate had little or no effect on cell growth. Uridine nucleotides, which inhibit galactosyltransferase activity, protected L1210 cells from the growth inhibitory effect of UDPgalactose when both were added simultaneously to culture media. Unlike mouse 3T12 cells, in which no inhibition of cell growth was observed with heat-inactivated calf serum (HICS)-DMEM, 5 mM UDPgalactose inhibited L1210 cell growth in HICS-DMEM to the same degree as that observed in CS-DMEM. In contrast to 3T12 cells, L1210 cells secrete significant galactosyltransferase activity into the media. Complete inhibition of 3T12 cell growth by UDPgal was observed if HICS-DMEM medium was first conditioned by L1210 cells for 48 hours. No difference in cell growth or [3H]thymidine uptake was detected after 6 hours of exposure to UDPgalactose, but both were significantly decreased at 24 and 48 hours. Flow cytometric analysis of UDPgalactose effects on L1210 cells revealed no differences in the distribution of cells in G1, S, or G2-M of the cell cycle after 6 hours of incubation, but after 16 hours of UDPgalactose treatment, L1210 cells were arrested in early S phase. These cells were completely viable and morphologically similar to control L1210 cells. Normal growth was resumed when UDPgal was removed. The data suggest that UDPgalactose inhibition of cell growth requires extracellular galactosyltransferase activity and that the effect is mediated via the cell membrane.

摘要

UDP-半乳糖抑制小鼠白血病L1210细胞的生长。在补充有小牛血清的杜尔贝科培养基(CS-DMEM)中,1.2 mM UDP-半乳糖(UDPgal)抑制细胞生长达50%(IC50),5 mM UDP-半乳糖抑制细胞生长达92%。其他核苷酸糖以及半乳糖、葡萄糖和1-磷酸半乳糖对细胞生长几乎没有影响或没有影响。抑制半乳糖基转移酶活性的尿苷核苷酸,当与UDP-半乳糖同时添加到培养基中时,可保护L1210细胞免受UDP-半乳糖的生长抑制作用。与小鼠3T12细胞不同,在热灭活小牛血清(HICS)-DMEM中未观察到细胞生长受到抑制,5 mM UDP-半乳糖在HICS-DMEM中对L1210细胞生长的抑制程度与在CS-DMEM中观察到的相同。与3T12细胞相反,L1210细胞向培养基中分泌显著的半乳糖基转移酶活性。如果先用L1210细胞对HICS-DMEM培养基预处理48小时,则观察到UDPgal对3T12细胞生长完全抑制。暴露于UDP-半乳糖6小时后,未检测到细胞生长或[3H]胸苷摄取的差异,但在24小时和48小时时两者均显著降低。流式细胞术分析UDP-半乳糖对L1210细胞的影响显示,孵育6小时后,细胞周期的G1、S或G2-M期细胞分布无差异,但UDP-半乳糖处理16小时后,L1210细胞停滞在S期早期。这些细胞完全存活,形态与对照L1210细胞相似。去除UDPgal后恢复正常生长。数据表明,UDP-半乳糖对细胞生长的抑制需要细胞外半乳糖基转移酶活性,且该效应是通过细胞膜介导的。

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Galactosyltransferase activity and cell growth: uridine diphosphate (UDP)galactose inhibition of murine leukemic L1210 cells.半乳糖基转移酶活性与细胞生长:尿苷二磷酸(UDP)半乳糖对小鼠白血病L1210细胞的抑制作用
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