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肿瘤细胞膜恶性表型及其逆转的实验研究

An experimental study on membrane malignant phenotype of tumour cells and their reversion.

作者信息

Yang Y Z, Zhang X H, Zhou R Z, Xia Q S, Liu L, Chen Z C

机构信息

Department of Medical Molecular Biology, Tongji Medical University, Wuhan.

出版信息

J Tongji Med Univ. 1994;14(1):7-11, 15. doi: 10.1007/BF02888049.

Abstract

A human promyelocytic leukemic cell line (HL-60 cells) was induced to differentiate along the myeloid pathway in vitro by 1.25% dimethylsulfoxide (DMSO) as an inducer. The membrane fluidity, the quantity of ConA binding sites on the cell membrane surface, and the protein tyrosine kinase (Tyr-PK) activity existing in NP-40 membrane extract and cytoplasma extract were determined respectively. The activity of tumour-derived immunosuppressive factor (TDSF) secreted by HL-60 cells into culture supernatant was also determined. The results demonstrated that: (1) HL-60 cells were capable of undergoing differentiation onto the myeloid pathway in the presence of DMSO. The growth of DMSO-treated HL-60 cells became slow and synthesis rate of DNA decreased by about 50%. (2) Both membrane fluidity and the quantity of ConA binding sites on membrane were obviously lower after induced with DMSO than those before induction. (3) The Tyr-PK activity in the NP-40 membrane extract increased during the period of induced differentiation. The phosphorylation level of endogenous protein in cytoplasma extract decreased with the process of induced differentiation. It may be reasoned that the phosphatase activity is much higher than the phosphorylase activity. (4) The secretive level of TDSF by HL-60 cells during the period of induced differentiation revealed no change. The preliminary results showed that the malignant phenotypes of tumour cells we used may undergo reversible changes with induced differentiation of tumour cells except the secretion of TDSF.

摘要

以1.25%二甲基亚砜(DMSO)作为诱导剂,在体外诱导人早幼粒细胞白血病细胞系(HL-60细胞)沿髓系途径分化。分别测定细胞膜流动性、细胞膜表面ConA结合位点数量以及NP-40膜提取物和细胞质提取物中存在的蛋白酪氨酸激酶(Tyr-PK)活性。还测定了HL-60细胞分泌到培养上清液中的肿瘤源性免疫抑制因子(TDSF)的活性。结果表明:(1)在DMSO存在下,HL-60细胞能够沿髓系途径分化。经DMSO处理的HL-60细胞生长变慢,DNA合成速率下降约50%。(2)经DMSO诱导后,细胞膜流动性和膜上ConA结合位点数量均明显低于诱导前。(3)在诱导分化期间,NP-40膜提取物中的Tyr-PK活性增加。随着诱导分化过程,细胞质提取物中内源性蛋白的磷酸化水平下降。可以推断磷酸酶活性远高于磷酸化酶活性。(4)HL-60细胞在诱导分化期间TDSF的分泌水平无变化。初步结果表明,除TDSF分泌外,我们所使用的肿瘤细胞的恶性表型可能随着肿瘤细胞的诱导分化而发生可逆变化。

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