The associated regulators and signal pathway in rIL-16/CD4 mediated growth regulation in Jurkat cells.
IL-16 is a ligand and chemotactic factor for CD4+ T cells. IL-16 inhibits the CD3 mediated lymphocyte activation and proliferation. The effects of IL-16 on the target cells are dependent on the cell type, the presence of co-activators etc. To understand the regulation function and mechanism of IL-16 on target cells, we used a 130 a.a. recombinant IL-16 to study its effects on the growth of Jurkat T leukemia cells in vitro. We found that the rIL-16 stimulated the proliferation of Jurkat cells at low dose (10(-9)M), but inhibited the growth of the cells at higher concentration (10(-5)M). Results showed that 10(-5) M of rIL-16 treatment induced an enhanced apoptosis in Jurkat cells. The treatment blocked the expression of FasL, but up-regulated the c-myc and Bid expression in the cells. Pre-treatment of PKC inhibitor or MEK1 inhibitor markedly increased or decreased the rIL-16 induced growth-inhibiting effects on Jurkat cells, respectively. The results suggested that the rIL-16 might be a regulator for the growth or apoptosis of Jurkat cells at a dose-dependent manner. The growth-inhibiting effects of rIL-16 might be Fas/FasL independent, but, associated with the activation of PKC, up-regulated expression of c-Myc and Bid, and the participation of the ERK signal pathway in Jurkat cells.
Zhang
Xiao Ming
XM
Lab of Molecular and Cellular Oncology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, 320 Yueyang Road, Shanghai 200031, China.
Xu
Yong Hua
YH
D017209:Apoptosis / Q000187:drug effects / Q000235:genetics / Q000276:immunology; D051023:BH3 Interacting Domain Death Agonist Protein; D015704:CD4 Antigens / Q000276:immunology* / Q000378:metabolism; D015496:CD4-Positive T-Lymphocytes / Q000187:drug effects / Q000276:immunology* / Q000378:metabolism; D002352:Carrier Proteins / Q000187:drug effects / Q000235:genetics / Q000276:immunology; D018797:Cell Cycle Proteins / Q000235:genetics / Q000276:immunology; D002455:Cell Division / Q000187:drug effects / Q000235:genetics / Q000276:immunology*; D004305:Dose-Response Relationship, Drug; D004791:Enzyme Inhibitors / Q000494:pharmacology; D053222:Fas Ligand Protein; D006801:Humans; D019410:Interleukin-16 / Q000235:genetics / Q000276:immunology* / Q000494:pharmacology; D019169:Jurkat Cells; D015458:Leukemia, T-Cell / Q000188:drug therapy / Q000276:immunology* / Q000378:metabolism; D020935:MAP Kinase Signaling System / Q000187:drug effects / Q000235:genetics / Q000276:immunology; D008562:Membrane Glycoproteins / Q000187:drug effects / Q000235:genetics / Q000276:immunology; D011493:Protein Kinase C / Q000187:drug effects / Q000235:genetics / Q000276:immunology; D016271:Proto-Oncogene Proteins c-myc / Q000187:drug effects / Q000235:genetics / Q000276:immunology; D011993:Recombinant Fusion Proteins / Q000494:pharmacology; D015398:Signal Transduction / Q000187:drug effects / Q000235:genetics / Q000276:immunology*
D051023:BH3 Interacting Domain Death Agonist Protein; C494814:BID protein, human; D015704:CD4 Antigens; D002352:Carrier Proteins; D018797:Cell Cycle Proteins; D004791:Enzyme Inhibitors; C505661:FASLG protein, human; D053222:Fas Ligand Protein; D019410:Interleukin-16; D008562:Membrane Glycoproteins; D016271:Proto-Oncogene Proteins c-myc; D011993:Recombinant Fusion Proteins; D011493:Protein Kinase C