Tsukuba Life Science Center, RIKEN (The Institute of Physical and Chemical Research), 3-1-1 Koyadai, Tsukuba, Ibaraki, 305-0074, Japan.
Cytotechnology. 2000 Jul;33(1-3):123-30. doi: 10.1023/A:1008129616127.
Mannosylerythritol lipid (MEL), an extracellularglycolipid from yeast, induces the differentiation ofHL-60 promyelocytic leukemia cells towardsgranulocytes. We show here that MEL is also a potentinhibitor of the proliferation of mouse melanoma B16cells. Flow-cytometric analysis of the cell cycle ofMEL-treated B16 cells revealed the accumulation ofcells in the sub-G(0)/G(1) phase, which is a hallmark ofcells undergoing apoptosis. Treatment of B16 cellsfor 24 h with phorbol 12-myristate 13-acetate (PMA),an activator of protein kinase C (PKC), did notinterfere with the growth and survival of the cells,but it effectively counteracted the MEL-induced growtharrest and apoptosis. The activity of PKC was reducedin B16 cells treated with MEL at a concentration atwhich MEL induced apoptosis. However, incubation withPMA in addition to MEL reversed this reduction in theactivity of PKC. These results suggest thatconverging signaling pathways are triggeredindependently by MEL and PMA and that the signalsmight both be mediated by PKC.
甘露糖赤藓糖醇脂质（MEL）是一种来自酵母的细胞外糖脂，可诱导 HL-60 早幼粒细胞白血病细胞向粒细胞分化。我们在这里表明，MEL 也是一种有效的小鼠黑色素瘤 B16 细胞增殖抑制剂。经 MEL 处理的 B16 细胞的细胞周期流式细胞术分析显示，细胞在亚 G0/G1 期积累，这是细胞凋亡的标志。用佛波醇 12-肉豆蔻酸 13-乙酸酯（PMA）处理 B16 细胞 24 小时，即蛋白激酶 C（PKC）的激活剂，不会干扰细胞的生长和存活，但可有效拮抗 MEL 诱导的生长停滞和细胞凋亡。用可诱导细胞凋亡的浓度的 MEL 处理 B16 细胞时，PKC 的活性降低。然而，在用 MEL 孵育的同时加入 PMA 可逆转 PKC 活性的降低。这些结果表明，MEL 和 PMA 独立触发趋同信号通路，并且这些信号可能都由 PKC 介导。
