Kaul D, Kaur M
Department of Experimental Medicine and Biotechnology, Postgraduate Institute of Medical Education and Research, Chandigarh, India.
Cancer Lett. 1997 Nov 11;119(2):131-5. doi: 10.1016/s0304-3835(97)00266-8.
Effect of low-density lipoprotein (LDL) on the expression of Bcl-2 as well as cyclin 'D' genes was studied in Receptor 'Ck' (+ve) and Receptor 'Ck'(-ve) human lymphocytes. LDL had no effect upon the elevated levels of Bcl-2 and cyclin 'D' gene products in Receptor 'Ck' (-ve) lymphocytes (from untreated CML patients), whereas in Receptor 'Ck' (+ve) lymphocytes (from normal subjects), the exposure to LDL regulated the level of cyclin 'D' gene product without initiating the expression of bcl-2 gene product. However, blockage of Receptor 'Ck' in normal lymphocytes, through its specific antibody (Ab-RCk) in presence or absence of LDL, resulted in the induction of both cyclin 'D' (at 4 h interval) and bcl-2 (at 12 h interval) gene products. Based upon these results, we propose that Receptor 'Ck' deficiency in cells may inherit defective apoptosis and capacity proliferation leading to leukemic transformation.
在受体“Ck”（阳性）和受体“Ck”（阴性）的人淋巴细胞中研究了低密度脂蛋白（LDL）对Bcl-2以及细胞周期蛋白“D”基因表达的影响。LDL对受体“Ck”（阴性）淋巴细胞（来自未经治疗的慢性粒细胞白血病患者）中升高的Bcl-2和细胞周期蛋白“D”基因产物水平没有影响，而在受体“Ck”（阳性）淋巴细胞（来自正常受试者）中，暴露于LDL可调节细胞周期蛋白“D”基因产物的水平，但不会启动bcl-2基因产物的表达。然而，在存在或不存在LDL的情况下，通过其特异性抗体（Ab-RCk）阻断正常淋巴细胞中的受体“Ck”，会导致细胞周期蛋白“D”（每隔4小时）和bcl-2（每隔12小时）基因产物的诱导。基于这些结果，我们提出细胞中受体“Ck”的缺陷可能会遗传有缺陷的细胞凋亡和增殖能力，从而导致白血病转化。
