Background. Eukaryotic translation initiation factor 3B (eIF3b) has been reported to be overexpressed in colon, bladder and prostate cancers as well as in glioblastoma. However, there is no report on any correlation of eIF3b gene expression with cell proliferation and apoptosis in chronic myeloid leukemia (CML). Objectives. In this study, we evaluated the role of eIF3b in cell proliferation and apoptosis in CML. Material and methods. Samples from patients with CML and CML cell lines were used. Quantitative RT-PCR, siRNA transfection, flow cytometry, and western blot analysis were performed. Results. Quantitative RT-PCR revealed that the expression of eIF3b mRNA in CML patients was higher than that in the non-malignant controls. The proliferation of CML cells decreased after transfection of the cells with siRNA. The proportion of cells in the G1 and S phases in the experimental group decreased after transfection, while the number of cells in the G2/M phase increased, as compared with the control group. The total cell apoptosis percentage in the sheIF3b group (transduction with lentivirus-anti-eIF3b in K562 cells) was higher than the shCtrl group (transduction with empty-vector lentivirus in K562 cells) after transfection. Caspase 3/7 activity was higher and the expression of anti-apoptotic protein BCL-2 was lower in the sheIF3b group than in the shCtrl group after transfection. Conclusions. Our results suggest that downregulation of eIF3b expression inhibits proliferation and induces apoptosis in CML cells.
To study the peripheral blood T-cell subsets and regulatory T-cells of multiple myeloma (MM) patients. 48 MM patients and 24 healthy controls were enrolled. Changes in peripheral blood T-cell subsets in the MM patients i.e. CD4 + CD25 + T cells and CD4 + CD25 + CD127 low T regulatory cells (CD4 + CD25 + CD127 low Tregs) and in healthy controls were measured using flow cytometry and immunohischemistry. The total T-cells (CD3 + ) in peripheral blood lymphocyte and auxiliary/ induced T-cells (CD3 + CD4 + T cell) of the 48 MM patients showed no statistical significance when compared with those of the control group. Suppressor/cytotoxicity T-cells (CD3 + CD8 + T cell) increased (p < 0.05). CD4 + CD25 + T cells and CD4 + CD25 + CD127 low Tregs were significantly higher than corresponding values in the healthy group (p < 0.05). The CD4 + /CD8 + T cell ratio of Stage III MM patients was significantly lower than that of the control group (p < 0.05). The CD4 + CD25 + T cells and CD4 + CD25 + CD127 low Tregs of MM patients in the stable and the progressive stages were significantly higher than those of MM patients in the control group (p < 0.05). The abnormality of the peripheral blood T-cell subset, increased expression of CD4 + CD25 + CD127 low Tregs, and low cellular immunity of MM patients are related to clinical staging and progression of the disease. The quantity of CD4 + CD25 + CD127 low Tregs of peripheral blood cells of MM patients could be significantly increased through the inhibition of CD4 + and CD8 + T cell activities. CD4 + CD25 + CD127 low Tregs promotes tumor growth through the inhibition of immunologic cell proliferation. Immunological dysfunction based on Tregs cells plays an important role in the pathogenic course.
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