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Volume 17,Issue 6,2010 Table of Contents
2010, 17(6):589-596.
DOI: 10.3872/j.issn.1007-385X.2010.6.001
Abstract:
In addition to the conventional therapeutic strategies, biotherapy also plays an important part in the treatment of hematopoietic malignancy (HM). According to the differentiation disorders of leukemia cells, HM should be treated by different differentiation inducers, which may induce them to differentiate into granulocytes, monocytes or DCs. Secondly, based on the key disease-associated genes, proteins, and cell surface antigen molecules in the pathogenesis of HM, new anti-HM drugs such as target antibody can be designed. Thirdly, based on the relationship of abnormalities of DNA methylation, chromosomes histone acetylation and histone deacetylation with the differentiation disorder of leukemia cells, some researchers studied the epigenetic modification of leukemia-associated genes and the therapeutic effects of anti-HM drugs regulating DNA methylation and histone acetylation. Last, tumor antigen or peptide specific tumor vaccines, cytokine/receptors-mediated target therapy, and partially-targeted cell vector-based therapy also have potential clinical applications. In conclusion, the differentiation inducers, key genes and molecule-targeted drugs and other target therapy agents all provide new ways for the treatment of HM; these agents used alone or in combination with other therapies will greatly enhance the treatment outcomes of HM.
In addition to the conventional therapeutic strategies, biotherapy also plays an important part in the treatment of hematopoietic malignancy (HM). According to the differentiation disorders of leukemia cells, HM should be treated by different differentiation inducers, which may induce them to differentiate into granulocytes, monocytes or DCs. Secondly, based on the key disease-associated genes, proteins, and cell surface antigen molecules in the pathogenesis of HM, new anti-HM drugs such as target antibody can be designed. Thirdly, based on the relationship of abnormalities of DNA methylation, chromosomes histone acetylation and histone deacetylation with the differentiation disorder of leukemia cells, some researchers studied the epigenetic modification of leukemia-associated genes and the therapeutic effects of anti-HM drugs regulating DNA methylation and histone acetylation. Last, tumor antigen or peptide specific tumor vaccines, cytokine/receptors-mediated target therapy, and partially-targeted cell vector-based therapy also have potential clinical applications. In conclusion, the differentiation inducers, key genes and molecule-targeted drugs and other target therapy agents all provide new ways for the treatment of HM; these agents used alone or in combination with other therapies will greatly enhance the treatment outcomes of HM.
2010, 17(6):597-603.
DOI: 10.3872/j.issn.1007-385X.2010.6.002
Abstract:
Objective : To investigate the methylation status in promoter and exon1 CpG island of Smad4 (mothers against decapentaplegic homolog 4) gene and its correlation with protein expressions of Smad4 and TGF-β1 in esophageal squamous cell carcinoma (ESCC). Methods: Totally 128 ESCC samples and the corresponding adjacent normal tissues were obtained from Fourth Hospital of Hebei Medical University (2004-2008) in the present study. Methylation specific PCR (MSP), RT-PCR and immunohistochemistry assays were used to examine the methylation status of 5′ CpG island, mRNA and protein expression of Smad4 in ESCC and the corresponding adjacent normal tissues. Immunohistochemistry method was used to detect the protein expression of TGF-β1 in ESCC and the corresponding adjacent normal tissues. Results: For the CpG island of promoter site, Smad4 was methylated in 7/128 (5.5%) ESCC tissues; for the CpG island of 5′ UTR of exon1, Smad4 was methylated in 39/128 (30.5%) ESCC tissues; the numbers were all significantly higher than those in the corresponding adjacent normal tissues (P<0.05). Smad4 mRNA and protein expressions in ESCC tissues were significantly lower than those in the corresponding adjacent normal tissues (P<0.05) and were correlated with Smad4 methylation status. TGF-β1 expression rate was 66.4% in ESCC tissues, which was significantly higher than that in the corresponding adjacent normal tissues (P<0.01), and TGF-β1 expression rate was increased with the increase of MNT stage and the decrease of differentiation stage of ESCC (P<0.05). The protein expression of Smad4 was inversely correlated with TGF-β1 expression in ESCC. Conclusion: Methylation of CpG island in Smad4 gene and TGF-β1 overexpression might play important roles in the development of ESCC, and CpG island in 5′ UTR of exon1 in Smad4 gene is more likely to be hypermethylated than the promoter region and results in Smad4 gene silence.
Objective : To investigate the methylation status in promoter and exon1 CpG island of Smad4 (mothers against decapentaplegic homolog 4) gene and its correlation with protein expressions of Smad4 and TGF-β1 in esophageal squamous cell carcinoma (ESCC). Methods: Totally 128 ESCC samples and the corresponding adjacent normal tissues were obtained from Fourth Hospital of Hebei Medical University (2004-2008) in the present study. Methylation specific PCR (MSP), RT-PCR and immunohistochemistry assays were used to examine the methylation status of 5′ CpG island, mRNA and protein expression of Smad4 in ESCC and the corresponding adjacent normal tissues. Immunohistochemistry method was used to detect the protein expression of TGF-β1 in ESCC and the corresponding adjacent normal tissues. Results: For the CpG island of promoter site, Smad4 was methylated in 7/128 (5.5%) ESCC tissues; for the CpG island of 5′ UTR of exon1, Smad4 was methylated in 39/128 (30.5%) ESCC tissues; the numbers were all significantly higher than those in the corresponding adjacent normal tissues (P<0.05). Smad4 mRNA and protein expressions in ESCC tissues were significantly lower than those in the corresponding adjacent normal tissues (P<0.05) and were correlated with Smad4 methylation status. TGF-β1 expression rate was 66.4% in ESCC tissues, which was significantly higher than that in the corresponding adjacent normal tissues (P<0.01), and TGF-β1 expression rate was increased with the increase of MNT stage and the decrease of differentiation stage of ESCC (P<0.05). The protein expression of Smad4 was inversely correlated with TGF-β1 expression in ESCC. Conclusion: Methylation of CpG island in Smad4 gene and TGF-β1 overexpression might play important roles in the development of ESCC, and CpG island in 5′ UTR of exon1 in Smad4 gene is more likely to be hypermethylated than the promoter region and results in Smad4 gene silence.
2010, 17(6):604-608.
DOI: 10.3872/j.issn.1007-385X.2010.6.003
Abstract:
Objective : To study the effect of siRNA targeting CHRNA5 (cholinergic receptor nicotinic alpha 5) gene expression on nicotine-induced proliferation of lung cancer A549 cells. Methods: CHRNA5-siRNA fragment was designed and synthesized, and then transfected into A549 cells by Lipofectamine assay. Expressions of CHRNA5 mRNA and protein in transfected-A549 cells were examined by FQ-PCR and Western blotting analysis, respectively. The effect of CHRNA5-siRNA on nicotine-induced proliferation of A549 cells was detected by MTT method. Results: CHRNA5-siRNA was successfully constructed and transfected into A549 cells. CHRNA5 mRNA expression in CHRNA5-siRNA-transfected A549 cells was significantly lower than that in control si-NC control siRNA transfected A549 cells (0.196±0.044 vs 0.944±0027, P<001), and CHRNA5 protein expression in CHRNA5-siRNA-transfected A549 cells was also lower than that in si-NC-transfected A549 cells (0.267±0.031 vs 0.745±0.035, P<0.01). When A549 cells were not treated with nicotine, CHRNA5-siRNA transfection inhibited the proliferation of A549 cells. But Nicotine increased the proliferation of A549 cells (P<0.01), and this positive effect was inhibited by CHRNA5-siRNA transfection (P<0.01). Conclusion: siRNA targeting CHRNA5 expression can inhibit nicotine-induced proliferation of A549 cells, which suggests that CHRNA5 may serve as a potential target for gene therapy of lung cancer.
Objective : To study the effect of siRNA targeting CHRNA5 (cholinergic receptor nicotinic alpha 5) gene expression on nicotine-induced proliferation of lung cancer A549 cells. Methods: CHRNA5-siRNA fragment was designed and synthesized, and then transfected into A549 cells by Lipofectamine assay. Expressions of CHRNA5 mRNA and protein in transfected-A549 cells were examined by FQ-PCR and Western blotting analysis, respectively. The effect of CHRNA5-siRNA on nicotine-induced proliferation of A549 cells was detected by MTT method. Results: CHRNA5-siRNA was successfully constructed and transfected into A549 cells. CHRNA5 mRNA expression in CHRNA5-siRNA-transfected A549 cells was significantly lower than that in control si-NC control siRNA transfected A549 cells (0.196±0.044 vs 0.944±0027, P<001), and CHRNA5 protein expression in CHRNA5-siRNA-transfected A549 cells was also lower than that in si-NC-transfected A549 cells (0.267±0.031 vs 0.745±0.035, P<0.01). When A549 cells were not treated with nicotine, CHRNA5-siRNA transfection inhibited the proliferation of A549 cells. But Nicotine increased the proliferation of A549 cells (P<0.01), and this positive effect was inhibited by CHRNA5-siRNA transfection (P<0.01). Conclusion: siRNA targeting CHRNA5 expression can inhibit nicotine-induced proliferation of A549 cells, which suggests that CHRNA5 may serve as a potential target for gene therapy of lung cancer.
2010, 17(6):609-614.
DOI: 10.3872/j.issn.1007-385X.2010.6.004
Abstract:
Objective : To observe the effects of signal regulatory protein α (SIRPα) on the adhesion, invasion and apoptosis of human breast cancer cells, and to explore the possible mechanism. Methods: SIRPα protein expression in high invasion breast cancer MDA-MB-231 cells and low invasion breast cancer MDA-MB-435 cells were detected by Western blotting analysis. pcDNA3.0-SIRPα plasmid was transfected into MDA-MB-231 cells by lipofectant assay, and SIRPα mRNA expression was examined by RT-PCR. Apoptosis of cells was examined by TUNEL method; invasion and adhesion abilities of MDA-MB-231 cells were examined by invasion or adhesion assays; and JNK and p-JNK protein expressions were determined by Western blotting analysis. Interaction of SIRPα with SHP2 in MDA-MB-435 cells stimulated with EGF was determined by immunoprecipitation assay. Results: Highly invasive MDA-MB-231 cells did not express SIRPα, while lowly invasive MDA-MB-435 cells expressed high level of SIRPα protein. pcDNA3.0-SIRPα transfection enhanced the adhesion of MDA-MB-231 cells, decreased their invasion ability, and promoted their apoptosis. Phosphorylation of JNK in pcDNA3.0-SIRPα transfected MDA-MB-231 cells was also decreased. EGF stimulation further increased SIRPα protein expression in MDA-MB-435 cells and enhanced the interaction of SIRPα with SHP2. Conclusion: SIRPα is related to adhesion and invasion of breast cancer cells, and might promote their apoptosis by decreasing the phosphorylation of JNK.
Objective : To observe the effects of signal regulatory protein α (SIRPα) on the adhesion, invasion and apoptosis of human breast cancer cells, and to explore the possible mechanism. Methods: SIRPα protein expression in high invasion breast cancer MDA-MB-231 cells and low invasion breast cancer MDA-MB-435 cells were detected by Western blotting analysis. pcDNA3.0-SIRPα plasmid was transfected into MDA-MB-231 cells by lipofectant assay, and SIRPα mRNA expression was examined by RT-PCR. Apoptosis of cells was examined by TUNEL method; invasion and adhesion abilities of MDA-MB-231 cells were examined by invasion or adhesion assays; and JNK and p-JNK protein expressions were determined by Western blotting analysis. Interaction of SIRPα with SHP2 in MDA-MB-435 cells stimulated with EGF was determined by immunoprecipitation assay. Results: Highly invasive MDA-MB-231 cells did not express SIRPα, while lowly invasive MDA-MB-435 cells expressed high level of SIRPα protein. pcDNA3.0-SIRPα transfection enhanced the adhesion of MDA-MB-231 cells, decreased their invasion ability, and promoted their apoptosis. Phosphorylation of JNK in pcDNA3.0-SIRPα transfected MDA-MB-231 cells was also decreased. EGF stimulation further increased SIRPα protein expression in MDA-MB-435 cells and enhanced the interaction of SIRPα with SHP2. Conclusion: SIRPα is related to adhesion and invasion of breast cancer cells, and might promote their apoptosis by decreasing the phosphorylation of JNK.
5 U87 glioma cell supernatant induces angiogenesis of CD133+ endothelial cells and possible mechanism
2010, 17(6):615-619.
DOI: 10.3872/j.issn.1007-385X.2010.6.005
Abstract:
Objective : To investigate the angiogenesis of CD133+ endothelial cells induced by glioma U87 cell supernatant and the possible mechanisms. Methods: CD133+ cells were sorted from the cord blood by magnetic activated cell sorting system, and were further induced to CD133+ endothelial cells. CD133+ endothelial cells were indetified by confocal microscopy and treated with U87 cell supernatant (DMEM used as control), and their angiogenesis and migration were examined by in vitro angiogenesis assay and Transwell assay, respectively. VEGFR-1, VEGFR-2 and MMP-9 (matrix metalloproteinase 9) expressions were determined by Western blotting analysis, and MMP-9 activity was examined by gelatin zymography assay. Results: After in vitro cultured for 14 d, the cord blood CD133+ cells showed positive expression of Dil-ac-LDL and FITC-UEA-1 and had the features of endothelial cells, so they were named CD133+ endothelial cells. The supernatant of U87 glioma cells induced tube formation of CD133+ endothelial cells and increased migration of CD133+ endothelial cells. U87 cell supernatant induced angiogenesis (\[40.7±3.3\] vs \[21±2.3\], P<0.05), increased migration (\[0.60±0.04\] vs \[0.27±002\], P<0.05), up-regulated VEGFR-2 and MMP-9 expressions (P<0.05) in CD133+ endothelial cells, while had minimal effect on VEGFR-1 expression. Moreover, U87 cell supernatant enhanced MMP-9 activity of CD133+ endothelial cells. Conclusion: Glioma U87 cell supernatant can induce angiogenesis of CD133+ endothelial cell via up-regulating VEGFR-2 and MMP-9 expressions.
Objective : To investigate the angiogenesis of CD133+ endothelial cells induced by glioma U87 cell supernatant and the possible mechanisms. Methods: CD133+ cells were sorted from the cord blood by magnetic activated cell sorting system, and were further induced to CD133+ endothelial cells. CD133+ endothelial cells were indetified by confocal microscopy and treated with U87 cell supernatant (DMEM used as control), and their angiogenesis and migration were examined by in vitro angiogenesis assay and Transwell assay, respectively. VEGFR-1, VEGFR-2 and MMP-9 (matrix metalloproteinase 9) expressions were determined by Western blotting analysis, and MMP-9 activity was examined by gelatin zymography assay. Results: After in vitro cultured for 14 d, the cord blood CD133+ cells showed positive expression of Dil-ac-LDL and FITC-UEA-1 and had the features of endothelial cells, so they were named CD133+ endothelial cells. The supernatant of U87 glioma cells induced tube formation of CD133+ endothelial cells and increased migration of CD133+ endothelial cells. U87 cell supernatant induced angiogenesis (\[40.7±3.3\] vs \[21±2.3\], P<0.05), increased migration (\[0.60±0.04\] vs \[0.27±002\], P<0.05), up-regulated VEGFR-2 and MMP-9 expressions (P<0.05) in CD133+ endothelial cells, while had minimal effect on VEGFR-1 expression. Moreover, U87 cell supernatant enhanced MMP-9 activity of CD133+ endothelial cells. Conclusion: Glioma U87 cell supernatant can induce angiogenesis of CD133+ endothelial cell via up-regulating VEGFR-2 and MMP-9 expressions.
2010, 17(6):620-624.
DOI: 10.3872/j.issn.1007-385X.2010.6.006
Abstract:
Objective : To investigate the inhibitory effect of triterpenes compound extracted from cortex periplocae (TCPP) on tumorigenesis of luciferase-marked Eca109 cells (Eca109, human esophageal cancer cell line; Eca109-luc) in nude mice and the related mechanisms. Methods: Eca109-luc-implanted tumor model was prepared by subcutaneously injecting Eca109-luc cells into nude mice. After treated with TCPP, the volume and weight of transplanted tumors in nude mice were measured, and tumor growth was monitored with in vivo imaging system. Morphology of transplanted tumor tissues was observed by H-E staining; apoptosis of transplanted tumor cells was analyzed by flow cytometry; and survivin expression in transplanted tumor tissues was examined by Western blotting analysis. Results: The growth of implanted tumor in nude mice was markedly inhibited by TCPP, and the volume and weight of tumors were significantly decreased, with the inhibitory rate being 40.7%. TCPP treatment induced inflammatory cell infiltration and necrosis of tumor cells in implanted tumor tissues, and the apoptosis rate of tumor cells was significantly higher than that in soybean oil control group (P<0.05). Expression level of survivin protein in implanted tumors was significantly lower in TCPP-treated group than that in control group (P<0.05). Conclusion: TCPP can inhibit proliferation of human esophageal cancer Eca109 cells in vivo, which might be associated with the down-regulation of survivin and apoptosis of tumor cells.
Objective : To investigate the inhibitory effect of triterpenes compound extracted from cortex periplocae (TCPP) on tumorigenesis of luciferase-marked Eca109 cells (Eca109, human esophageal cancer cell line; Eca109-luc) in nude mice and the related mechanisms. Methods: Eca109-luc-implanted tumor model was prepared by subcutaneously injecting Eca109-luc cells into nude mice. After treated with TCPP, the volume and weight of transplanted tumors in nude mice were measured, and tumor growth was monitored with in vivo imaging system. Morphology of transplanted tumor tissues was observed by H-E staining; apoptosis of transplanted tumor cells was analyzed by flow cytometry; and survivin expression in transplanted tumor tissues was examined by Western blotting analysis. Results: The growth of implanted tumor in nude mice was markedly inhibited by TCPP, and the volume and weight of tumors were significantly decreased, with the inhibitory rate being 40.7%. TCPP treatment induced inflammatory cell infiltration and necrosis of tumor cells in implanted tumor tissues, and the apoptosis rate of tumor cells was significantly higher than that in soybean oil control group (P<0.05). Expression level of survivin protein in implanted tumors was significantly lower in TCPP-treated group than that in control group (P<0.05). Conclusion: TCPP can inhibit proliferation of human esophageal cancer Eca109 cells in vivo, which might be associated with the down-regulation of survivin and apoptosis of tumor cells.
2010, 17(6):625-629.
DOI: 10.3872/j.issn.1007-385X.2010.6.007
Abstract:
Objective : To study the effects of IL-2, IFN-α and IFN-γ on B7-H1 expression in renal clear cell carcinoma 786-0 cells. Methods: 786-0 cells were stimulated with IL-2, IFN-α and IFN-γ; the expression of B7-H1 mRNA was examined by RT-PCR; and the expression of B7-H1 protein was detected by immunocytochemistry staining, immunofluorescence staining, and flow cytometry assay. Results: RT-PCR results showed that B7-H1 mRNA expression was higher in 786-0 cells stimulated with IL-2, IFN-α, and IFN-γ compared with those in unstimulated cells (0.75±0.06,0.68±005, 0.95±0.08 vs 0.30±0.03, P﹤0.05). B7-H1 protein was distributed in the cell membrane as showed by immunocytochemistry and immunofluorescence staining, and the expression of B7-H1 protein was up-regulated after IL-2, IFN-α, and IFN-γ stimulation. Flow cytometry results showed that B7-H1 protein expressions in 786-0 cells stimulated with IL-2, IFN-α, and IFN-γ were significantly higher than that in unstimulated cells (\[65.70±3.26\]%, \[56.52±175\]%, \[84.05±3.52\]% vs \[20.49±1.03\]%, P<0.01). Conclusion: IL-2, IFN-α and IFN-γ can all up-regulate the expression of B7-H1 mRNA and protein in 786-0 cells, with IFN-γ showing the most potent up-regulation effect and IFN-α showing the least one.
Objective : To study the effects of IL-2, IFN-α and IFN-γ on B7-H1 expression in renal clear cell carcinoma 786-0 cells. Methods: 786-0 cells were stimulated with IL-2, IFN-α and IFN-γ; the expression of B7-H1 mRNA was examined by RT-PCR; and the expression of B7-H1 protein was detected by immunocytochemistry staining, immunofluorescence staining, and flow cytometry assay. Results: RT-PCR results showed that B7-H1 mRNA expression was higher in 786-0 cells stimulated with IL-2, IFN-α, and IFN-γ compared with those in unstimulated cells (0.75±0.06,0.68±005, 0.95±0.08 vs 0.30±0.03, P﹤0.05). B7-H1 protein was distributed in the cell membrane as showed by immunocytochemistry and immunofluorescence staining, and the expression of B7-H1 protein was up-regulated after IL-2, IFN-α, and IFN-γ stimulation. Flow cytometry results showed that B7-H1 protein expressions in 786-0 cells stimulated with IL-2, IFN-α, and IFN-γ were significantly higher than that in unstimulated cells (\[65.70±3.26\]%, \[56.52±175\]%, \[84.05±3.52\]% vs \[20.49±1.03\]%, P<0.01). Conclusion: IL-2, IFN-α and IFN-γ can all up-regulate the expression of B7-H1 mRNA and protein in 786-0 cells, with IFN-γ showing the most potent up-regulation effect and IFN-α showing the least one.
2010, 17(6):630-633.
DOI: 10.3872/j.issn.1007-385X.2010.6.008
Abstract:
Objective : To investigate the effects of different polysaccharides isolated from Se-enriched spirulina platensis (Se-PSP) on the growth of tumor cells. Methods: Crude total sugar Se-PSP and its different components (Se-PSP1, Se-PSP2, Se-PSP3 and Se-PSP4) were extracted from se-enriched spirulina (Se-SP) by ultrasonic method, and four Se-PSP components were further isolated and purified by DEAE-cellulose column. The effects of total sugar Se-PSP and four different components (10 μg/ml) on the growth of SKOV-3 cells, and different concentrations of Se-PSP2 on the growth of SKOV-3 cells, HepG-2 cells, BGC-803 cells, CNE cells and Tca-8113 cells were examined by MTT method. Results: Four different components (Se-PSP1, Se-PSP2, Se-PSP3 and Se-PSP4) were isolated and purified from Se-PSP, with Se-PSP2 being the most abundant one. The inhibitory rates of Se-PSP and four different components (Se-PSP1, Se-PSP2, Se-PSP3 and Se-PSP4) on growth of SKOV-3 cells were (33.393±5.437)%, (22.290±8.399)%, (44.881±4.878)%, (45.354±4931)% and (46.203±4.455) %, respectively, with the inhibitory rates of Se-PSP2, Se-PSP3 and Se-PSP4 being significantly higher than those of Se-PSP and Se-PSP1 (P<0.05), but those of Se-PSP2, Se-PSP3 and Se-PSP4 showing no difference (P>0.05). Se-PSP2 dose-dependently inhibited the proliferation of SKOV-3, HepG-2, BGC-803 and Tca-8113 cells (all P<0.05), and showed broad anti-tumor spectra. Conclusion: Se-PSP2 is the main component of Se-PSP, and it can inhibit the growth of various types of tumor cells, making it a promising adjuvant drug for treatment of malignant tumors.
Objective : To investigate the effects of different polysaccharides isolated from Se-enriched spirulina platensis (Se-PSP) on the growth of tumor cells. Methods: Crude total sugar Se-PSP and its different components (Se-PSP1, Se-PSP2, Se-PSP3 and Se-PSP4) were extracted from se-enriched spirulina (Se-SP) by ultrasonic method, and four Se-PSP components were further isolated and purified by DEAE-cellulose column. The effects of total sugar Se-PSP and four different components (10 μg/ml) on the growth of SKOV-3 cells, and different concentrations of Se-PSP2 on the growth of SKOV-3 cells, HepG-2 cells, BGC-803 cells, CNE cells and Tca-8113 cells were examined by MTT method. Results: Four different components (Se-PSP1, Se-PSP2, Se-PSP3 and Se-PSP4) were isolated and purified from Se-PSP, with Se-PSP2 being the most abundant one. The inhibitory rates of Se-PSP and four different components (Se-PSP1, Se-PSP2, Se-PSP3 and Se-PSP4) on growth of SKOV-3 cells were (33.393±5.437)%, (22.290±8.399)%, (44.881±4.878)%, (45.354±4931)% and (46.203±4.455) %, respectively, with the inhibitory rates of Se-PSP2, Se-PSP3 and Se-PSP4 being significantly higher than those of Se-PSP and Se-PSP1 (P<0.05), but those of Se-PSP2, Se-PSP3 and Se-PSP4 showing no difference (P>0.05). Se-PSP2 dose-dependently inhibited the proliferation of SKOV-3, HepG-2, BGC-803 and Tca-8113 cells (all P<0.05), and showed broad anti-tumor spectra. Conclusion: Se-PSP2 is the main component of Se-PSP, and it can inhibit the growth of various types of tumor cells, making it a promising adjuvant drug for treatment of malignant tumors.
2010, 17(6):634-638.
DOI: 10.3872/j.issn.1007-385X.2010.6.009
Abstract:
Objective : To investigate the effect IL-27 on apoptosis of human pancreatic carcinoma Aspc1 cells and its in vivo anti-tumor activity. Methods: PA317/IL-27 retrovirus vector was transfected into Aspc1 cells and the stable clones (Aspc1/IL-27) were obtained by selecting with G418. The effects of IL-27 on production of IL-27, proliferation, and MHC-Ⅰ expression of Aspc1 cells were determined by ELISA, cell counting and flow cytometry, respectively. Aspc1/IL-27, Aspc1/LXSN (Aspc1 cells stably transfected with empty vector) and Aspc1 cells were subcutaneously injected into nude mice, and the growth of transplanted tumors and survival time of mice were observed. Apoptosis and ultramicrostructure of the implanted-tumor cells were examined by TUNEL and electron microscope respectively. Results: Aspc1 cells stably transfected with PA317/IL-27 (Aspc1/IL-27) were successfully prepared. Aspc1/IL-27 cells secreted high levels of IL-27, while Aspc1/IL-27 and Aspc1 cells did not secreted IL-27 (P<0.01). Aspc1/IL-27 transfection did not affect the expression of MHC-Ⅰ on Aspc1 cells (P>0.05). The growth of implanted-tumors was significantly slower and the survival time was longer in Aspc1/IL-27 group than those in Aspc1/LXSN and Aspc1 groups (P<0.05). Apoptosis rate of implanted-tumor cells in Aspc1/IL-27 cells was significantly higher than those in Aspc1/LXSN and Aspc1 groups (\[19.5±2.4\]%, \[8.5±0.3\]%, \[9.1±0.8\]%, P<0.01) . Conclusion: IL-27 gene transfection exerts in vivo anti-tumor activity by inducing apoptosis of human pancreatic carcinoma cells.
Objective : To investigate the effect IL-27 on apoptosis of human pancreatic carcinoma Aspc1 cells and its in vivo anti-tumor activity. Methods: PA317/IL-27 retrovirus vector was transfected into Aspc1 cells and the stable clones (Aspc1/IL-27) were obtained by selecting with G418. The effects of IL-27 on production of IL-27, proliferation, and MHC-Ⅰ expression of Aspc1 cells were determined by ELISA, cell counting and flow cytometry, respectively. Aspc1/IL-27, Aspc1/LXSN (Aspc1 cells stably transfected with empty vector) and Aspc1 cells were subcutaneously injected into nude mice, and the growth of transplanted tumors and survival time of mice were observed. Apoptosis and ultramicrostructure of the implanted-tumor cells were examined by TUNEL and electron microscope respectively. Results: Aspc1 cells stably transfected with PA317/IL-27 (Aspc1/IL-27) were successfully prepared. Aspc1/IL-27 cells secreted high levels of IL-27, while Aspc1/IL-27 and Aspc1 cells did not secreted IL-27 (P<0.01). Aspc1/IL-27 transfection did not affect the expression of MHC-Ⅰ on Aspc1 cells (P>0.05). The growth of implanted-tumors was significantly slower and the survival time was longer in Aspc1/IL-27 group than those in Aspc1/LXSN and Aspc1 groups (P<0.05). Apoptosis rate of implanted-tumor cells in Aspc1/IL-27 cells was significantly higher than those in Aspc1/LXSN and Aspc1 groups (\[19.5±2.4\]%, \[8.5±0.3\]%, \[9.1±0.8\]%, P<0.01) . Conclusion: IL-27 gene transfection exerts in vivo anti-tumor activity by inducing apoptosis of human pancreatic carcinoma cells.
2010, 17(6):639-643.
DOI: 10.3872/j.issn.1007-385X.2010.6.010
Abstract:
Objective : To explore the roles of heparanase (HPSE) in the invasion and metastasis of human ovarian carcinoma A2780 cells. Methods: pcDNA3.1-HPSE eukaryotic expression vector was constructed. pcDNA3.1-HPSE and empty pcDNA3.1 plasmids were transfected into A2780 cells by Lipofectamine method, and A2780 cells stably expressing pcDNA3.1-HPSE or pcDNA3.1 were selected by G418 (named pcDNA3.1-HPSE-A2780 or pcDNA3.1-A2780 cells). The proliferation of A2780 cells after pcDNA3.1-HPSE transfection was detected by MTT and clone-forming experiment, and the invasion, migration and adhesion capacities of A2780 cells were tested by Matrigel, Transwell and Adhersion assays, respectively. Results: The pcDNA3.1-HPSE vector was successfully constructed and transfected into A2780 cells. pcDNA3.1-HPSE transfection had no effect on proliferation and migration of A2780 cells (all P>0.05). pcDNA3.1-HPSE transfection increased invasion (0.477±0.024 vs 0.250±0.081, P=0.003) and inhibited the adhesion of A2780 cells (0.728±0.089 vs 0.518±0.080, P=0.002). Conclusion: Heparanase plays important roles in ovarian carcinoma by promoting invasion and inhibiting adhesion of tumor cells.
Objective : To explore the roles of heparanase (HPSE) in the invasion and metastasis of human ovarian carcinoma A2780 cells. Methods: pcDNA3.1-HPSE eukaryotic expression vector was constructed. pcDNA3.1-HPSE and empty pcDNA3.1 plasmids were transfected into A2780 cells by Lipofectamine method, and A2780 cells stably expressing pcDNA3.1-HPSE or pcDNA3.1 were selected by G418 (named pcDNA3.1-HPSE-A2780 or pcDNA3.1-A2780 cells). The proliferation of A2780 cells after pcDNA3.1-HPSE transfection was detected by MTT and clone-forming experiment, and the invasion, migration and adhesion capacities of A2780 cells were tested by Matrigel, Transwell and Adhersion assays, respectively. Results: The pcDNA3.1-HPSE vector was successfully constructed and transfected into A2780 cells. pcDNA3.1-HPSE transfection had no effect on proliferation and migration of A2780 cells (all P>0.05). pcDNA3.1-HPSE transfection increased invasion (0.477±0.024 vs 0.250±0.081, P=0.003) and inhibited the adhesion of A2780 cells (0.728±0.089 vs 0.518±0.080, P=0.002). Conclusion: Heparanase plays important roles in ovarian carcinoma by promoting invasion and inhibiting adhesion of tumor cells.
2010, 17(6):644-647.
DOI: 10.3872/j.issn.1007-385X.2010.6.011
Abstract:
Objective : To study the effect of microRNA-17-5p (miR-17-5p) on the growth of chronic myelocytic leukemia K562 cells by antisense oligonucleocide technique. Methods： miR-17-5p antisense oligonucleotide (miR-17-5p-ASO) and control nonsense oligonucleotide (Ctrl-NSO) were transfected into K562 cells by Lipofectamine assay, and un-transfected K562 cells were used as blank group (Ctrl). The proliferation, apoptosis, and cell cycle changes of K562 cells were examined by MTT, TUNEL, and flow cytometry assays, respectively. Results: MTT results showed that the proliferation of K562 cells in miR-17-5p-ASO group was (61.7±4.7)% of that in Ctrl-NSO group, and miR-17-5p-ASO transfection significantly inhibited the proliferation of K562 cells (P<0.05). TUNEL results showed that miR-17-5p-ASO transfection did not affect apoptosis of K562 cells (P>0.05). The ratio of K562 cells in G2 phase was (10.8±08)％ in miR-17-5p-ASO group, which was significantly lower that those in Ctrl-NSO and Ctrl groups (\[34.6±04\]%, \[33.9±1.3\]%, all P<0.05). Conclusion: MiR-17-5p specific antisense oligonucleotide can suppress K562 cells growth by inhibiting cell cycle, which may provide a new way for treatment of leukemia.
Objective : To study the effect of microRNA-17-5p (miR-17-5p) on the growth of chronic myelocytic leukemia K562 cells by antisense oligonucleocide technique. Methods： miR-17-5p antisense oligonucleotide (miR-17-5p-ASO) and control nonsense oligonucleotide (Ctrl-NSO) were transfected into K562 cells by Lipofectamine assay, and un-transfected K562 cells were used as blank group (Ctrl). The proliferation, apoptosis, and cell cycle changes of K562 cells were examined by MTT, TUNEL, and flow cytometry assays, respectively. Results: MTT results showed that the proliferation of K562 cells in miR-17-5p-ASO group was (61.7±4.7)% of that in Ctrl-NSO group, and miR-17-5p-ASO transfection significantly inhibited the proliferation of K562 cells (P<0.05). TUNEL results showed that miR-17-5p-ASO transfection did not affect apoptosis of K562 cells (P>0.05). The ratio of K562 cells in G2 phase was (10.8±08)％ in miR-17-5p-ASO group, which was significantly lower that those in Ctrl-NSO and Ctrl groups (\[34.6±04\]%, \[33.9±1.3\]%, all P<0.05). Conclusion: MiR-17-5p specific antisense oligonucleotide can suppress K562 cells growth by inhibiting cell cycle, which may provide a new way for treatment of leukemia.
2010, 17(6):648-652.
DOI: 10.3872/j.issn.1007-385X.2010.6.012
Abstract:
Objective : To prepare recombinant BALF4 poptein of VCA (viral capsid antigen) in Epstein-Barr virus and analyze its application in detection of nasopharyngeal carcinoma (NPC). Methods: BALF4 gene was amplified from EBV DNA sequence by PCR and then inserted into pPICZαA pichia pastoris expression vector. Recombinant pPICZαA-BALF4 plasmid was transfected into GS115 yeast cells, and corresponding recombinant BALF4 protein was induced by methanol. The recombinant BALF4 protein was identified by SDS-PAGE and Western blotting analysis, and used as coating antigen for detection of EBV-IgA antibody in NPC patients by ELISA. Results: pPICZαA-BALF4 expression vector was succesffuly constructed, and recombinant BALF4 protein was effectively expressed GS115 yeast cells. The molecular weight of recombinant BALF4 protein is approximately 52 000, and the recombinant BALF4 protein showed good immunoreactivity as detected by Western blotting analysis. Recombinant BALF4 protein was used as coating antigen in detecting EBV-IgA antibody levels in serum samples collected from NPC patients and healthy controls, and the sensitivity and specificity of VCA-BALF4 in the test were 81% and 94%, respectively. Conclusion: The recombinant BALF4 protein has been succesffuly prepared and it has satisfying sensitivity and specificity in serum screening of NPC patients.
Objective : To prepare recombinant BALF4 poptein of VCA (viral capsid antigen) in Epstein-Barr virus and analyze its application in detection of nasopharyngeal carcinoma (NPC). Methods: BALF4 gene was amplified from EBV DNA sequence by PCR and then inserted into pPICZαA pichia pastoris expression vector. Recombinant pPICZαA-BALF4 plasmid was transfected into GS115 yeast cells, and corresponding recombinant BALF4 protein was induced by methanol. The recombinant BALF4 protein was identified by SDS-PAGE and Western blotting analysis, and used as coating antigen for detection of EBV-IgA antibody in NPC patients by ELISA. Results: pPICZαA-BALF4 expression vector was succesffuly constructed, and recombinant BALF4 protein was effectively expressed GS115 yeast cells. The molecular weight of recombinant BALF4 protein is approximately 52 000, and the recombinant BALF4 protein showed good immunoreactivity as detected by Western blotting analysis. Recombinant BALF4 protein was used as coating antigen in detecting EBV-IgA antibody levels in serum samples collected from NPC patients and healthy controls, and the sensitivity and specificity of VCA-BALF4 in the test were 81% and 94%, respectively. Conclusion: The recombinant BALF4 protein has been succesffuly prepared and it has satisfying sensitivity and specificity in serum screening of NPC patients.
2010, 17(6):653-656.
DOI: 10.3872/j.issn.1007-385X.2010.6.013
Abstract:
Objective : To investigate the expressions of RhoA and Ezrin in breast infiltrating ductal carcinoma (BIDC) and their clinical significances. Methods: Eighty-six BIDC paraffin samples were obtained from Fourth Hospital of Hebei Medical University (Jan. 2008 to Dec. 2008). Immunohistochemical method was used to assess the expression of RhoA and Ezrin in tumor tissues. The relationship between RhoA and Ezrin expressions with the clinicopathological parameters was also analyzed. Results: The expression of RhoA and the strong expression of Ezrin in the 86 BIDC samples were 6047% and 65.12%, respectively, which were both significantly higher than those in normal ductal epithelium groups (all P<0.05). Neither the expression of RhoA nor the strong expression of Ezrin was correlated with patient’s age (P>0.05), and they were positively correlated with the axillary lymph node metastasis, histological grades, and TNM stages (all P<0.05). A significant correlation was also found between the expression of RhoA and the strong expression of Ezrin in BIDC samples (P<0.01). Conclusion: RhoA and Ezrin are highly expressed in IBDC tissues, and may play important roles in the carcinogenesis and progression of BIDC.
Objective : To investigate the expressions of RhoA and Ezrin in breast infiltrating ductal carcinoma (BIDC) and their clinical significances. Methods: Eighty-six BIDC paraffin samples were obtained from Fourth Hospital of Hebei Medical University (Jan. 2008 to Dec. 2008). Immunohistochemical method was used to assess the expression of RhoA and Ezrin in tumor tissues. The relationship between RhoA and Ezrin expressions with the clinicopathological parameters was also analyzed. Results: The expression of RhoA and the strong expression of Ezrin in the 86 BIDC samples were 6047% and 65.12%, respectively, which were both significantly higher than those in normal ductal epithelium groups (all P<0.05). Neither the expression of RhoA nor the strong expression of Ezrin was correlated with patient’s age (P>0.05), and they were positively correlated with the axillary lymph node metastasis, histological grades, and TNM stages (all P<0.05). A significant correlation was also found between the expression of RhoA and the strong expression of Ezrin in BIDC samples (P<0.01). Conclusion: RhoA and Ezrin are highly expressed in IBDC tissues, and may play important roles in the carcinogenesis and progression of BIDC.
LIU Li-min
,
ZHANG Yan-ming
,
LU Shu-hua
,
SUN Yu-mei
,
ZHAO Guang-sheng
,
ZHANG Xing-xia
,
CUI Hong-xia
2010, 17(6):657-660.
DOI: 10.3872/j.issn.1007-385X.2010.6.014
Abstract:
Objective : To explore the effect of astragalus polysaccharide (APS) on maturation of plasmacytoid dendritic cells (pDCs) from acute myeloid leukemia (AML) patients. Methods: Twenty-three AML patients from Second People’s Hospital of Huai’an City (Oct. 2009 to Feb. 2010) were used in this study. Peripheral mononuclear cells were obtained and were sorted by flow cytometry. pDCs were then stimulated with APS for 5 days; their phenotypes were analyzed by flow cytometry, morphology was observed under light microscope, and ultrastructure was observed under scanning electron microscope. pDCs were treated with different concentrations of APS (0, 50, 100, 200 μg/ml) for 24 h, and IFN-α, TNF-α and IL-6 levels in pDC supernatants were examined by ELISA. Results: Light microscope and scanning electron microscope results showed that APS-treated pDCs displayed mature morphology with more and longer dendritic spines. APS promoted differentiation and maturation of pDC by increasing the positive rates of CD11c, CD80 and CD86 in a dose-dependent manner (P＜0.05). APS also dose-dependently up-regulated IFN-α, TNF-α, and IL-6 secretion in pDCs (P＜005). Conclusion: APS can enhance the function of pDCs of AML patients, and promote their differentiation and maturation.
Objective : To explore the effect of astragalus polysaccharide (APS) on maturation of plasmacytoid dendritic cells (pDCs) from acute myeloid leukemia (AML) patients. Methods: Twenty-three AML patients from Second People’s Hospital of Huai’an City (Oct. 2009 to Feb. 2010) were used in this study. Peripheral mononuclear cells were obtained and were sorted by flow cytometry. pDCs were then stimulated with APS for 5 days; their phenotypes were analyzed by flow cytometry, morphology was observed under light microscope, and ultrastructure was observed under scanning electron microscope. pDCs were treated with different concentrations of APS (0, 50, 100, 200 μg/ml) for 24 h, and IFN-α, TNF-α and IL-6 levels in pDC supernatants were examined by ELISA. Results: Light microscope and scanning electron microscope results showed that APS-treated pDCs displayed mature morphology with more and longer dendritic spines. APS promoted differentiation and maturation of pDC by increasing the positive rates of CD11c, CD80 and CD86 in a dose-dependent manner (P＜0.05). APS also dose-dependently up-regulated IFN-α, TNF-α, and IL-6 secretion in pDCs (P＜005). Conclusion: APS can enhance the function of pDCs of AML patients, and promote their differentiation and maturation.
2010, 17(6):661-664.
DOI: 10.3872/j.issn.1007-385X.2010.6.015
Abstract:
Objective : To observe the short-term efficacy and toxicity of Endostar combined with image guided radiation therapy (IGRT) in treatment of non-small-cell lung cancer (NSCLC) patients with brain metastasis. Methods： Forty NSCLC patients with brain metastasis, who were treated in the Department of Oncology of Provincial Hospital of Hebei during Jan. 2008 to Jun. 2008, were enrolled in the present study, and were randomly divided into trial group (22 cases) and control group (18 cases). The trial group received Endostar combined with IGRT (Endostar+IGRT group) and the control group received only IGRT at the same dosage (IGRT group). The short-term efficacy was evaluated by RESICT criteria and toxicity was evaluated according to NCI CTC Version 3.0 criteria. Results: The overall response rate was 773% in Endostar+IGRT group versus 61.1% in IGRT group (P<0.05). The clinical benefit rates in the Endostar+IGRT group and IGRT group were 90.9% and 72.2%, respectively (P<0.05). The main toxicities were leucopenia, nausea/vomiting and acratia, and their incidences in Endostar+IGRT group were similar to those in IGRT group (P>005). The median free time to progression was 11.6 months in the Endostar+IGRT group and 11.3 months in the IGRT group (P>0.05); the one year survival rates were 54.5% and 55.6%, respectively, with no difference between the two groups (P>0.05). Conclusion: Endostar combined with IGRT can increase the total effective rate and clinical benefit of NSCLC patients with brain metastasis.
Objective : To observe the short-term efficacy and toxicity of Endostar combined with image guided radiation therapy (IGRT) in treatment of non-small-cell lung cancer (NSCLC) patients with brain metastasis. Methods： Forty NSCLC patients with brain metastasis, who were treated in the Department of Oncology of Provincial Hospital of Hebei during Jan. 2008 to Jun. 2008, were enrolled in the present study, and were randomly divided into trial group (22 cases) and control group (18 cases). The trial group received Endostar combined with IGRT (Endostar+IGRT group) and the control group received only IGRT at the same dosage (IGRT group). The short-term efficacy was evaluated by RESICT criteria and toxicity was evaluated according to NCI CTC Version 3.0 criteria. Results: The overall response rate was 773% in Endostar+IGRT group versus 61.1% in IGRT group (P<0.05). The clinical benefit rates in the Endostar+IGRT group and IGRT group were 90.9% and 72.2%, respectively (P<0.05). The main toxicities were leucopenia, nausea/vomiting and acratia, and their incidences in Endostar+IGRT group were similar to those in IGRT group (P>005). The median free time to progression was 11.6 months in the Endostar+IGRT group and 11.3 months in the IGRT group (P>0.05); the one year survival rates were 54.5% and 55.6%, respectively, with no difference between the two groups (P>0.05). Conclusion: Endostar combined with IGRT can increase the total effective rate and clinical benefit of NSCLC patients with brain metastasis.
2010, 17(6):665-667.
DOI: 10.3872/j.issn.1007-385X.2010.6.016
Abstract:
目的： 分析人宫颈癌组织中表皮生长因子受体基因（epidermal growth factor receptor，EGFR）突变的发生和突变类型，为临床针对EGFR的靶向治疗宫颈癌提供实验依据。 方法： 选取86例宫颈癌患者的病理组织石蜡标样，采用酚氯仿法抽提基因组DNA，分别采用聚合酶链反应（polymerase chain reaction，PCR）技术及聚合酶链反应-限制性片段长度多态分析（restriction fragment length polymorphism-polymerase chain reaction，PCR-RLFP）检测人宫颈癌组织EGFR基因是否存在第19外显子的缺失突变及第21外显子的点突变。 结果： 在86例人宫颈癌组织标本中，PCR未检测到EGFR基因第19外显子的缺失突变，PCR-RLFP 未检测到EGFR基因第 21外显子的点突变。 结论： 人宫颈癌组织EGFR基因中未检测到第19外显子缺失突变和第21外显子的点突变。
目的： 分析人宫颈癌组织中表皮生长因子受体基因（epidermal growth factor receptor，EGFR）突变的发生和突变类型，为临床针对EGFR的靶向治疗宫颈癌提供实验依据。 方法： 选取86例宫颈癌患者的病理组织石蜡标样，采用酚氯仿法抽提基因组DNA，分别采用聚合酶链反应（polymerase chain reaction，PCR）技术及聚合酶链反应-限制性片段长度多态分析（restriction fragment length polymorphism-polymerase chain reaction，PCR-RLFP）检测人宫颈癌组织EGFR基因是否存在第19外显子的缺失突变及第21外显子的点突变。 结果： 在86例人宫颈癌组织标本中，PCR未检测到EGFR基因第19外显子的缺失突变，PCR-RLFP 未检测到EGFR基因第 21外显子的点突变。 结论： 人宫颈癌组织EGFR基因中未检测到第19外显子缺失突变和第21外显子的点突变。
2010, 17(6):668-672.
DOI: 10.3872/j.issn.1007-385X.2010.6.017
Abstract:
单核细胞与树突状细胞系细胞在血液中循环并最终迁移到组织中，它们在组织中进一步成熟并发挥免疫防御等多种功能。近年来，采用流式细胞术对这些细胞的表面标志分子特征进行了详细的分析，发现了相应的细胞亚群。国际免疫学会命名委员会（由英国莱斯特大学免疫学研究所Loems Ziegler-Heitbrock教授为首的18位科学家组成）对这些细胞进行了统一命名，将人和小鼠血液单核细胞分为三种类型：经典型（classical monocytes）、中间型（intermediate monocytes）和非经典型单核细胞（non-classical monocytes）；将人和小鼠血液树突状细胞也分为三种类型：浆细胞样(plasmacytoid dendritic cells)和两类髓样树突状细胞（myeloid dendritic cells)。目前该分类及其命名已被国际免疫学会批准，该命名将更好地促进科学家之间甚至是学科之间更广泛的交流。
单核细胞与树突状细胞系细胞在血液中循环并最终迁移到组织中，它们在组织中进一步成熟并发挥免疫防御等多种功能。近年来，采用流式细胞术对这些细胞的表面标志分子特征进行了详细的分析，发现了相应的细胞亚群。国际免疫学会命名委员会（由英国莱斯特大学免疫学研究所Loems Ziegler-Heitbrock教授为首的18位科学家组成）对这些细胞进行了统一命名，将人和小鼠血液单核细胞分为三种类型：经典型（classical monocytes）、中间型（intermediate monocytes）和非经典型单核细胞（non-classical monocytes）；将人和小鼠血液树突状细胞也分为三种类型：浆细胞样(plasmacytoid dendritic cells)和两类髓样树突状细胞（myeloid dendritic cells)。目前该分类及其命名已被国际免疫学会批准，该命名将更好地促进科学家之间甚至是学科之间更广泛的交流。
2010, 17(6):673-677.
DOI: 10.3872/j.issn.1007-385X.2010.6.018
Abstract:
Imatinib, a tyrosine kinase inhibitor, is one of the major drugs for treating gastrointestinal stromal tumor (GIST). However, some patients suffer severe cardiotoxicity after imatinib treatment, with unclear mechanism. Studies have suggested that the different signal transduction pathways mediated by the endoplasmic reticulum stress play a central role in imatinib-induced cardiactoxicity, and these signal pathways can interact with the mitochondrial signal pathway through c-Abl. Competitive binding of imatinib to the ATP binding site in tyrosine kinase domain cause abnormal myocardial energy metabolism and increase oxidative stress, and the sustained oxidative stress lead to abnormal expression of c-Abl and phosphorylation of PDGFR, meanwhile, c-Abl and PDGFR-mediated signal transduction pathway abnormalities is closely associated with imatinib induced cardiotoxicity.
Imatinib, a tyrosine kinase inhibitor, is one of the major drugs for treating gastrointestinal stromal tumor (GIST). However, some patients suffer severe cardiotoxicity after imatinib treatment, with unclear mechanism. Studies have suggested that the different signal transduction pathways mediated by the endoplasmic reticulum stress play a central role in imatinib-induced cardiactoxicity, and these signal pathways can interact with the mitochondrial signal pathway through c-Abl. Competitive binding of imatinib to the ATP binding site in tyrosine kinase domain cause abnormal myocardial energy metabolism and increase oxidative stress, and the sustained oxidative stress lead to abnormal expression of c-Abl and phosphorylation of PDGFR, meanwhile, c-Abl and PDGFR-mediated signal transduction pathway abnormalities is closely associated with imatinib induced cardiotoxicity.
2010, 17(6):678-682.
DOI: 10.3872/j.issn.1007-385X.2010.6.019
Abstract:
MicroRNA (miRNA), an important post-transcriptional regulator, is involved in a variety of physical and pathological processes, including the development of immune cells and inflammation response. Among them, miR-155, miR-17～92, miR-146a, miR-150, and miR-181a are extremely important. MiR-155 is an essential regulator for T and B cell differentiation and antibody class switch of B cells, miR-17～92 is associated with the development of B cells, miR-150 negatively regulates the development of B cells and inflammation response, miR-181a participates in the development of T cells, and miR-146a is a negative regulator of inflammatory response. Further understanding of the regulatory function of miRNA on immune cells and their mechanisms will promote immunology research and its application in the prevention and treatment of immuno-related diseases.
MicroRNA (miRNA), an important post-transcriptional regulator, is involved in a variety of physical and pathological processes, including the development of immune cells and inflammation response. Among them, miR-155, miR-17～92, miR-146a, miR-150, and miR-181a are extremely important. MiR-155 is an essential regulator for T and B cell differentiation and antibody class switch of B cells, miR-17～92 is associated with the development of B cells, miR-150 negatively regulates the development of B cells and inflammation response, miR-181a participates in the development of T cells, and miR-146a is a negative regulator of inflammatory response. Further understanding of the regulatory function of miRNA on immune cells and their mechanisms will promote immunology research and its application in the prevention and treatment of immuno-related diseases.
2010, 17(6):683-686.
DOI: 10.3872/j.issn.1007-385X.2010.6.020
Abstract:
In recent years, the role of chemokines in tumor growth and metastasis have been attracting greater attention worldwide. Studies on breast cancer, prostate cancer and pancreatic cancer have revealed that CXCL12/CXCR4 axis can increase the growth, inhibit the apoptosis, promote the angiogenesis, affect the targeted metastasis, enhance the adhesion and migration, and regulate the cytokine secretion of tumor cells, which indicates CXCL12/CXCR4 axis may be a new target for antitumor drugs and plays a potential role in clinical tumor therapy.
In recent years, the role of chemokines in tumor growth and metastasis have been attracting greater attention worldwide. Studies on breast cancer, prostate cancer and pancreatic cancer have revealed that CXCL12/CXCR4 axis can increase the growth, inhibit the apoptosis, promote the angiogenesis, affect the targeted metastasis, enhance the adhesion and migration, and regulate the cytokine secretion of tumor cells, which indicates CXCL12/CXCR4 axis may be a new target for antitumor drugs and plays a potential role in clinical tumor therapy.
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Supported by:Beijing E-Tiller Technology Development Co., Ltd.