脂氧素对K562和HL-60白血病细胞增殖和凋亡的影响(英文)

Effects of Lipoxin A_4 on Proliferation and Apoptosis of K562 and HL-60 Leukemic Cells

炎症在肿瘤的发生发展过程中扮演重要角色,脂氧素是一类重要的内源性抗炎介质。但是迄今为止,脂氧素对肿瘤的影响报道极少。为此,本文研究了脂氧素对HL-60和K562白血病细胞增殖和凋亡的影响。体外培养白血病细胞株HL-60和K562,Western印迹和实时荧光定量PCR检测脂氧素受体的表达情况;CCK-8法(cell counting kit-8 assay)检测HL-60和K562的增殖能力;PI染色后利用流式细胞仪进行细胞周期分析;膜联蛋白V试剂盒检测脂氧素对细胞凋亡的影响。实验结果表明脂氧素抑制HL-60和K562白血病细胞增殖(P<0.05);脂氧素处理组S期细胞比例明显减少而G_0/G_1期细胞比例增加;脂氧素还可以诱导HL-60和K562白血病细胞凋亡。由此可见,脂氧素抑制HL-60和K562白血病细胞增殖,其机制可能与诱导白血病细胞G_0/G_1期阻滞和细胞凋亡有关。

Inflammation is a critical component of tumour progression. Lipoxins （LXs） are approved for potent anti-inflammatory properties. However, there are few reports dealing with their effects on cancer. In this study, we tested their effects on HL-60 and K562 leukemia cells. Western blot and real time PCR were used to examine the expression of lipoxin A4 receptor （ALX）. Cellular proliferation and cycle were determined via cell counting kit-8 assay （CCK-8） and propidium iodide staining. Apoptosis was assessed by the annexin V assay. We discovered LXs inhibited the proliferation of HL-60 and K562 cells, increased the number of cells in G0/G1 phase, decreased that in S phase, and induced the apoptosis of HL-60 and K562 cells. It hinted LXs inhibited the proliferation of HL-60 and K562 cells and the mechanism might be associated with cell cycle arrest in G0/G1 phase and induction of apoptosis.