Receptor-Ck-dependent regulation of genes in HL-60 cell line.
The selective and conspicuous absence of a novel receptor-Ck (having affinity for cholesterol moiety in lipoproteins and intrinsic tyrosine kinase activity) in various leukemic cell lines/patients, prompted us to explore the nature of interrelationship between receptor-Ck deficiency and over-expression of genes coding for bcl-2, cyclin 'D', chimeric bcr-abl, c-myc and LDL-receptor in the human promyelocytic leukemic cell line (HL-60). This study revealed unambiguously that deregulated expression of these genes is primarily due to the inability of these cells to express the receptor-Ck gene. Based upon the observations we propose that 'receptor-Ck' deficiency may be responsible for the initiation of chronic myeloid leukemia.
Kaul
D
D
Department of Experimental Medicine & Biotechnology, Postgraduate Institute of Medical Education & Research, Chandigarh, India.
Kaur
M
M
D002784:Cholesterol / Q000378:metabolism / Q000494:pharmacology; D056741:Cyclin D; D016213:Cyclins / Q000096:biosynthesis / Q000235:genetics; D016044:Fusion Proteins, bcr-abl / Q000096:biosynthesis / Q000235:genetics; D015973:Gene Expression Regulation, Leukemic / Q000502:physiology*; D019254:Genes, bcl-2; D016259:Genes, myc; D018922:HL-60 Cells / Q000502:physiology* / Q000648:ultrastructure*; D006801:Humans; D008081:Liposomes; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000096:biosynthesis / Q000235:genetics; D016271:Proto-Oncogene Proteins c-myc / Q000096:biosynthesis; D018110:Receptors, Lipoprotein / Q000096:biosynthesis / Q000172:deficiency / Q000235:genetics / Q000502:physiology*
D056741:Cyclin D; D016213:Cyclins; D008081:Liposomes; D019253:Proto-Oncogene Proteins c-bcl-2; D016271:Proto-Oncogene Proteins c-myc; D018110:Receptors, Lipoprotein; C072413:apolipoprotein B receptor; D002784:Cholesterol; D016044:Fusion Proteins, bcr-abl