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机构地区:[1]第四军医大学西京医院血液科,西安710032
出 处:《中国肿瘤生物治疗杂志》1996年第1期48-50,共3页Chinese Journal of Cancer Biotherapy
摘 要:采用0.5%~1.0%低血清培养法较好地模拟了小剂量rhTNF-α(50U/ml)对人早幼粒白血病细胞株HL-60的增殖抑制效应,但未发现促分化作用,对细胞株c-myc基因的表达亦无明显影响;而TNF(50μ/ml)具有诱导HL-60细胞分化和抑制细胞增殖的作用,且显著抑制其c-myc癌基因的表达水平。结果表明c-myc基因表达减低主要与TNF诱导HL-60白血病细胞分化相关,并非细胞增殖受抑的结果,对癌基因表达水平的调控可能是小剂量TNF发挥分化诱导作用的重要机制。We compared the changes of c-myc expression, cell growth kinetics, ability to reduce NBT and 3H -TdR incorporation rate of HL-60 cells in low concentration of FCS, or treated by TNF or no treatment, respectively. The results showed that, although the prolifcrative suppression of HL-60 cells treated by 50U/ml TNF was mimicked by adding 1. 0%and 0. 5%FCS in culture media, the differentiation had notappeared and it had not effected on c - myc expression, either. TNF (50U/ml) could inhibit proliferation of HL-60 cells during inducing differentiation and the expression of c-myc oncogene decreased remarkedly. The results indicated that decreased expression of c-myc in TNF treated HL-60 cells were mainly connected with differentiate maturation but not with proliferative suppression.
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