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Objective To investigate the role of CRKL activity in leukemia cells with muhidrug resistance and find new factor related to multidrug resistance. Methods By flow cytometry, CRKL activity was compared in K562, HL-60 cells and its resistance cells. The change of CRKL activity was observed in sensitive cells treated with and withdrawal daunorubicin. Results With the comparison of K562, HL-60 sensitive cells, in K562, HL-60 resistant cell lines, the level of CRKL phosphorylation in K562, HL-60 resistance cells treated with daunombicin 72 hours increased markedly. The level of CRKL phosphorylation was time-dependent with chemotherapy drugs, not change of CRKL activity was found in Jurkat ceils.Conclusion The level of CRKL activity is new factor related to muhidrug resistance in leukemia cells.
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Objective To explore the mechanism and way for CT10 regulator of kinase like (CRKL) involving in drug resistance in leukemia cells. Methods The four major proteins included Ras protein, signal transducer and activator of transcripton 5 (STAT5) protein, phosphoinositide 3-kinase (PI3K) protein and paxillin protein in leukemia which involved in signal transduction pathway of CRKL. The expressions of those proteins were detected by Western-blot and immunofluorescent staining and confocal laser scanning microscopy. Results Compared with K562/S cells, the expressions of Ras(41.52±15.47 vs. 23.74±8.67) and PI3K (35.60±12.48 vs. 10.09±0.005) protein were up-regulated in K562/ADM cells (t=3.01,6.13;both P<0.05), while there were no significant changes in the expressions of paxillin (20.10±11.89 vs. 23.11±12.40) and STAT5 protein (25.72±14.46 vs. 17.58±9.21) between K562/S cells and K562/ADM cells(t=0. 18,1.43;both P>0. 0S). Conclusions Ras and PI3K protein may play a role in the multidrug resistance of K562 cell line, while paxillin and STAT5 protein may be not involved in the formation of resistant in K562 cells.
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Objective: To study the relation among inducible nitric oxide synthase(iNOS), endothelial nitric oxide synthase(eNOS) and vascular endothelial growth factor (VEGF)in oral squamous cell carcinoma(OSCC) and their relation to clinical pathology and angiogenesis.Methods:OSCC tissue specimens were surgically obtained from 64 patients,the expression of iNOS,eNOS and VEGF in the samples were studied by immunohistochemistry technique. Microvessel density(MVD) was measured by counting the endothelial cells stained with anti-FⅧRAg antibody. Results: ①Positive VEGF and iNOS and eNOS immunostaining was detected in 39(60.94%),42(65.63%)and 45( 70.31%)of the cases respectively.②Expression of VEGF was significantly related to that of iNOS(P05).③MVD in OSCC tissue was positively correlated with the expression of VEGF and iNOS(P05).④VEGF expression was positively correlated to the pathological grade of OSCC(P0.05).Conclusion:iNOS,rather than eNOS, plays a positive role in OSCC development.iNOS and VEGF have a positive correlation in angiogenesis of OSCC.