Induction of Erythroid-Specific Genes by Overexpression of GATA-2 in K562 Cells
Hideo HarigaeYoko OkitsuHisayuki YokoyamaTohru FujiwaraMitsue InomataShinichiro TakahashiNaoko MinegishiMitsuo KakuTakeshi Sasaki
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Hematology
K562 cells
Objective: To investigate the regulation of p-glycoprotein (PgP) and GST expression from three reversors in ADM-sensitive and ADM-resistant human leukemic cell lines and KB cell lines. Methods: Immunocytochemical(ICC) technique was applied to detect the multidrug-resistant gene products, PgP and GST in K562 cells, K562/ADM cells and KB cells before or after treatment with three resistant reversors, i.e., verapamil(VER), dipyriamole(DPM) and cyclosporin A(CsA). Results: PgP expression was observed in K562/ADM cells but not in K562 cells or KB cells, and GSTPI expression, in KB cells but not in K562 cells or K562/ADM cells. Overexpressions of PgP were induced after treatment with VER, or DPM or CsA for 24 h in K562 cells but not KB cells. DPM-treated K562/ADM cells expressed PgP much lower than DPM-ree of K562/ADM cells with CsA for 24 h. Induced GSTPI expression was found after treatment with DPM, but not VER or CsA in K562 cells. No significant difference was observed for GSTPI expresion in KB cells before and after treatment with VER, or DPM, or CsA. Conclusion: The findings suggested that reversal activity of some drug resistant reversors, such as VER, DPM, CsA, may be declined by themselves through induction of PgP, perhaps GST.
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P-glycoprotein
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Objective To investigate the different effect of Sorafenib and TRAIL on proliferationinhibition and apoptosis inducing of K562 cells.Methods Inhibition of K562 cells proliferationby Sorafenib alone and combined with TRAIL were studied in vitro using CCK-8. Apoptosis induc-ing rate of K562 cells by Sorafenib alone and combined with TRAIL were accessed by Western-Blotdetection.Results Combination with Sorafenib and TRAIL synergistically increased the growthinhibition effects and enhanced the apoptosis rate of K562 cells.Conclusion Combination treat-ment of Sorafenib and TRAIL showed a synergistic anti-proliferative effect in K562 cells.
K562 cells
Growth inhibition
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Objective To investigate the role of SHP1 gene in inducing apoptosis and erythroid differentiation in human erythromyeloblastoid leukemia cell line K562.Methods The full length cDNA of SHP1 gene was cloned by RT-PCR and was subcloned into mammalian expression vector pcDNA3.0.The cDNA sequence of the cloned gene was validated by enzyme digestion and DNA sequencing.Then the recombinant plasmid was used to transfect K562 cells via lipofectin.The apoptosis of K562 cells was examined by Hoechst 33258 staining assay and Annexin Ⅴ/PI double-labeled assay;the differentiation of K562 cells was observed by benzidine staining and expression of glycophorin A (GPA).Results RT-PCR and Western blotting analysis showed expression of SHP1 in K562 cells after transfection with pcDAN3-SHP1 plasmid.Apoptotic cells were detected in the K562 cells 48 h after treatment with pcDNA3-SHP1,with the apoptosis rate being 16.84%,which was significantly higher than that in cells transfected with pcDNA3.0 (6.23%,P=0.000).The positive rate of benzidine staining was 14.67% and the positive rate of GPA expression was 19.38% in cells treated with pcNDA3-SHP1,both were significantly different from those in the cells transfected with pcDNA3.0 (P=0.005).Conclusion Over-expression of SHP1 can effectively induce apoptosis and erythroid differentiation in K562 cells.
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We describe an exemplary case of inadequate health legislation and defensive medicine, regarding umbilical cord tissue collection for personal "private" use.
Hematology
Blood cell
Blood Disorder
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Objective:To examine the expression of Smad7 gene and protein in human chronic myelogenous leukemia cell line (K562) and to explore the effects of TGF-β1 on the expression of Smad7 preliminaryly. Method:We studied the expression of Smad7 gene and protein in K562 cell line and the alteration of Smad7 after incubated with TGF-β1 by RT-PCR analysis, western blot. Result:The expression of Smad7 was detected in K562 cell line,and can be induced by the stimulation of TGF-β1 transiently. The expression of Smad7 and the alteration of Smad7 after TGF-β1 treatment at the translational level generally parallel to those at the transcriptional level. Conclusion:Smad7 Participates in the TGF-β signal transduction of K562 cell line.There's a negative auto-regulatory feedback loop between Smad7 and TGF-β1.
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Chronic myelogenous leukemia
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We previously isolated aaptamine, a benzonaphthyridine alkaloid, from marine sponge Aaptos suberitoids. In this study, we investigated the anti-proliferative effect of aaptamine on chronic myeloid leukemia (CML) K562 cells. Aaptamine inhibited growth of K562 with a GI50 as 10 μM, and arrested cell cycle at G2/M phase. Western blot analysis indicated that aaptamine induced p21 expression in K562 cells. Moreover, p21 promoter was activated by aaptamine treatment in p21 transfected K562 cells. Since K562 is p53 negative, aaptamine was demonstrated to be a p53-independent p21 inducer in CML cells.
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Homology
R gene
Conserved sequence
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Hematology (also spelled haematology) is the branch of medicine concerned with the study of the cause, prognosis, treatment, and prevention of diseases related to blood. The blood plays an essential roles in human health
Hematology
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Hematology
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Transfusion medicine
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BACKGROUND AND AIM:To investigate the effect of cortex periplocae extract(CPE) on the differentiation of tumor cells K562 in vitro.MATERIALS AND METHODS:We examined the morphological changes of K562 cells after cultured with CPE;and investigated the induction effect of CPE on the production of Hb from K562 cells by using colorimetry.RESULTS:K562 cells morphology were destroyed by CPE.CPE also markedly reduced the production of Hb from K562 cells.CONCLUSION:CPE could kill K562 cells to some extent,but could not induce the differentiation of K562 cells.
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Colorimetry
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