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Volume 10,Issue 4,2003 Table of Contents
2003, 10(4):239-242.
DOI: 10.3872/j.issn.1007-385X.2003.4.002
Abstract:
Objective：To investigate the anti-tumor effects of anti-hCGβ antibody induced by gene immunization with ectopic human chorionic gonadotropin β-subunit. Methods：Sera were collected at the indicated times from the mice immunized with plasmid TR421-ehCGβ-coding for hCGβ and mock DNA respectively and were determined the levels of anti-hCGβ antibody by ELISA. The tumor cells expressing ehCGβ were treated with different doses of sera, in which complement were or not inactivated. The proliferation and morphological change as well as apoptosis of tumor cells were detected by \[3H\]-Thymidine incorporation assay, converse-microscope and FACS, respectively. Results：All mice immunized with plasmid TR421-ehCGβ developed high levels of anti-hCGβ antibody, which could inhibit obviously the proliferation of Hela cells compared with the serum from animals immunized with mock DNA (P<0.05), even if complement was inactivated. However, the inhibition of normal serum decreased significantly after complement was inactivated. The inhibition activity of the anti-hCGβ serum correlated with the expression level of ehCGβ in the tumor cells. The number of dead Hela cells increased obviously upon being incubated with the anti-hCGβ serum, while the percentage of the apoptotic cells was only 3.42%, which had no significant difference with the cells incubated with the normal serum (1.88%). Conclusion：The anti-hCGβ antibody induced by gene immunization had significant inhibitory influence on the proliferation of tumor cells expression ehCGβ in complement-independent manner.
Objective：To investigate the anti-tumor effects of anti-hCGβ antibody induced by gene immunization with ectopic human chorionic gonadotropin β-subunit. Methods：Sera were collected at the indicated times from the mice immunized with plasmid TR421-ehCGβ-coding for hCGβ and mock DNA respectively and were determined the levels of anti-hCGβ antibody by ELISA. The tumor cells expressing ehCGβ were treated with different doses of sera, in which complement were or not inactivated. The proliferation and morphological change as well as apoptosis of tumor cells were detected by \[3H\]-Thymidine incorporation assay, converse-microscope and FACS, respectively. Results：All mice immunized with plasmid TR421-ehCGβ developed high levels of anti-hCGβ antibody, which could inhibit obviously the proliferation of Hela cells compared with the serum from animals immunized with mock DNA (P<0.05), even if complement was inactivated. However, the inhibition of normal serum decreased significantly after complement was inactivated. The inhibition activity of the anti-hCGβ serum correlated with the expression level of ehCGβ in the tumor cells. The number of dead Hela cells increased obviously upon being incubated with the anti-hCGβ serum, while the percentage of the apoptotic cells was only 3.42%, which had no significant difference with the cells incubated with the normal serum (1.88%). Conclusion：The anti-hCGβ antibody induced by gene immunization had significant inhibitory influence on the proliferation of tumor cells expression ehCGβ in complement-independent manner.
2 The Affecting Factors of Inducing Human Peripheral Blood Monocyte-Derived Dendritic Cells in vitro
SHU Yong-qian
,
ZHU Yi-bei
,
DAI Jun
,
XI Hong
,
HUANG Yong
,
WU Ming-yuan
,
XIA Yu
,
ZHANG Xue-guang
2003, 10(4):243-247.
DOI: 10.3872/j.issn.1007-385X.2003.4.003
Abstract:
Objective：To study the affecting factors on the differentiation, maturation and function on the human peripheral blood monocyte-derived dendritic cells (DC). Methods：Through DCs′ surface molecules analysis, mixed-lymphocyte reaction, FITC-Dextran capture, cell counting and chemotaxis activity of T lymphocytes, we compared functions of DC stimulated with different cytokines including TNF-α, FL, sCD40L, CD40mAb,gp130 and IL-10. Results：Both CD40- and TNF-α signalling are able to promote differentiation and maturation of DC, including upregulation of costimulatory molecules expression, such as CD80 and CD86, enhancement of DC-mediated MLR, promotion of T cell chemotactic ability to DC; CD40 signalling counteracted the inhibitory effects of IL-10 on DC more efficiently than TNF-α signalling; The agonist gp130 mAb and human recombinant FL can remarkably promote the proliferation of DC in vitro, while there are no distinct effects on DCs′ differentiation, maturation and ability to activate T cells.Conclusions： CD40 signalling is more powerful than TNF-α, and plays a unique role to abtain more mature and functional DC in vitro.
Objective：To study the affecting factors on the differentiation, maturation and function on the human peripheral blood monocyte-derived dendritic cells (DC). Methods：Through DCs′ surface molecules analysis, mixed-lymphocyte reaction, FITC-Dextran capture, cell counting and chemotaxis activity of T lymphocytes, we compared functions of DC stimulated with different cytokines including TNF-α, FL, sCD40L, CD40mAb,gp130 and IL-10. Results：Both CD40- and TNF-α signalling are able to promote differentiation and maturation of DC, including upregulation of costimulatory molecules expression, such as CD80 and CD86, enhancement of DC-mediated MLR, promotion of T cell chemotactic ability to DC; CD40 signalling counteracted the inhibitory effects of IL-10 on DC more efficiently than TNF-α signalling; The agonist gp130 mAb and human recombinant FL can remarkably promote the proliferation of DC in vitro, while there are no distinct effects on DCs′ differentiation, maturation and ability to activate T cells.Conclusions： CD40 signalling is more powerful than TNF-α, and plays a unique role to abtain more mature and functional DC in vitro.
2003, 10(4):248-252.
DOI: 10.3872/j.issn.1007-385X.2003.4.004
Abstract:
Objective:To observe the respective effects of Tju103 and CTLA4-Ig on tolerance, post haploidentical mice bone marrow transplantation. Methods:In the presence of the recipient antigen, T cells from the haploidentical donors were first cultured with Tju103 or CTLA4-Ig, then mixed with the bone marrow cells and transfused into the recipients. At last, they were observed on the effect on tolerance post transplantation. Results: A. The only irradiated group: All the mice died of failure of hematopoiesis within 11 days post irradiation. B. The CTX-treated leukemia group: All the mice died of leukemia within 16-23 days. C.The only transplanted group: All cases died of GVHD within 21 days post transplantation. D. The CsA prophylaxis group: 5 mice died within 8-22 days after transplantation, of which one died of leukemia, and two died of GVHD and infection respectively leaving 5 survived over 30 days post transplantation. E. The Tju103 treated group: 4 mice died within 9-26 days post transplantation, of which one died of leukemia and infection respectively, and two died of GVHD leaving 6 mice survived over 30 days post transplantation. F. The CTLA4-Ig treated group: 2 mice died of GVHD within 17~26 days after transplantation leaving 8 survived over 30 days post transplantation. Conclusions:Tju103 or CTLA4-Ig could alone improve survival time and reduce incidence and degree of GVHD respectively. But CTLA4-Ig could preserve ability of GVL effect and anti-infection potential while Tju103 couldn′t.
Objective:To observe the respective effects of Tju103 and CTLA4-Ig on tolerance, post haploidentical mice bone marrow transplantation. Methods:In the presence of the recipient antigen, T cells from the haploidentical donors were first cultured with Tju103 or CTLA4-Ig, then mixed with the bone marrow cells and transfused into the recipients. At last, they were observed on the effect on tolerance post transplantation. Results: A. The only irradiated group: All the mice died of failure of hematopoiesis within 11 days post irradiation. B. The CTX-treated leukemia group: All the mice died of leukemia within 16-23 days. C.The only transplanted group: All cases died of GVHD within 21 days post transplantation. D. The CsA prophylaxis group: 5 mice died within 8-22 days after transplantation, of which one died of leukemia, and two died of GVHD and infection respectively leaving 5 survived over 30 days post transplantation. E. The Tju103 treated group: 4 mice died within 9-26 days post transplantation, of which one died of leukemia and infection respectively, and two died of GVHD leaving 6 mice survived over 30 days post transplantation. F. The CTLA4-Ig treated group: 2 mice died of GVHD within 17~26 days after transplantation leaving 8 survived over 30 days post transplantation. Conclusions:Tju103 or CTLA4-Ig could alone improve survival time and reduce incidence and degree of GVHD respectively. But CTLA4-Ig could preserve ability of GVL effect and anti-infection potential while Tju103 couldn′t.
2003, 10(4):253-256.
DOI: 10.3872/j.issn.1007-385X.2003.4.005
Abstract:
Objective: To study the effect of cell proliferation transfected with tumor associated antigen encoding gene CHP2. Methods: Using PCR method to clone CHP2 encoding gene and inserting it into the eukaryotic expression vector pcDNA3 to construct the recombination pcDNA-CHP2. The fusion gene was identified by enzyme digestion and DNA sequencing. 293 cells transfected CHP2 genes were selected by G418 pressure and the cell proliferation was measured by 3-TdR uptake. Results: Identified by enzyme digestion and sequencing, CHP2 gene was correctly cloned into pcDNA3. The results of the western blot showed the transfected cell could express CHP2 protein. 3-TdR uptake value of the CHP2 transfected cell was lower than the control. Conclusions: CHP2 could inhibit cell proliferation and it maybe an important regulator involved in cell proliferation.
Objective: To study the effect of cell proliferation transfected with tumor associated antigen encoding gene CHP2. Methods: Using PCR method to clone CHP2 encoding gene and inserting it into the eukaryotic expression vector pcDNA3 to construct the recombination pcDNA-CHP2. The fusion gene was identified by enzyme digestion and DNA sequencing. 293 cells transfected CHP2 genes were selected by G418 pressure and the cell proliferation was measured by 3-TdR uptake. Results: Identified by enzyme digestion and sequencing, CHP2 gene was correctly cloned into pcDNA3. The results of the western blot showed the transfected cell could express CHP2 protein. 3-TdR uptake value of the CHP2 transfected cell was lower than the control. Conclusions: CHP2 could inhibit cell proliferation and it maybe an important regulator involved in cell proliferation.
WANG Ying
,
YOU Qiang
,
ZHANG Hui-zhen
,
WANG Shu-jun
,
CHEN Lin lin
,
ZHOU Guang-yan
,
GE Hai-liang
2003, 10(4):257-259.
DOI: 10.3872/j.issn.1007-385X.2003.4.006
Abstract:
Objective: To establish the methods for screening the HLA-A2-restricted peptides on T2-dependent cell model. Methods: The binding ability and binding stability of peptides to HLA-A2 molecule was determined by measuring peptide-induced expression of HLA-A2 molecules on TAP-deficient cell line-T2 cells. Briefly, T2 cells were incubated with OVA66 candidate peptides at different concentration(0.2 μg/ml, 2 μg/ml, 5 μg/ml, 20 μg/ml) and different time. After incubation, expression of HLA-A2 molecules on T2 cells was detected by flow cytometry with murine mAb BB7.2 against human HLA-A2 molecule. The binding ability of peptides was calculated with peptide concentration of 20% MFImax, while the binding stability of peptides was calculated with percentage of MFI(4h)/MFI(0 h).Results: Four OVA66 candidate peptides were assayed with this method. Compared with reference peptide, two peptides (L235 and L238) displayed strong binding ability and good stability, while other two peptides (L236 and L237) exhibited low affinity to HLA-A2 molecules on T2 cells. Conclusion: With T2-dependent cell model, we could test the binding ability and binding stability of peptides before inducing peptide-specific T cell lines in vitro.
Objective: To establish the methods for screening the HLA-A2-restricted peptides on T2-dependent cell model. Methods: The binding ability and binding stability of peptides to HLA-A2 molecule was determined by measuring peptide-induced expression of HLA-A2 molecules on TAP-deficient cell line-T2 cells. Briefly, T2 cells were incubated with OVA66 candidate peptides at different concentration(0.2 μg/ml, 2 μg/ml, 5 μg/ml, 20 μg/ml) and different time. After incubation, expression of HLA-A2 molecules on T2 cells was detected by flow cytometry with murine mAb BB7.2 against human HLA-A2 molecule. The binding ability of peptides was calculated with peptide concentration of 20% MFImax, while the binding stability of peptides was calculated with percentage of MFI(4h)/MFI(0 h).Results: Four OVA66 candidate peptides were assayed with this method. Compared with reference peptide, two peptides (L235 and L238) displayed strong binding ability and good stability, while other two peptides (L236 and L237) exhibited low affinity to HLA-A2 molecules on T2 cells. Conclusion: With T2-dependent cell model, we could test the binding ability and binding stability of peptides before inducing peptide-specific T cell lines in vitro.
2003, 10(4):260-264.
DOI: 10.3872/j.issn.1007-385X.2003.4.007
Abstract:
Objective: To explore the inhibitory effect of algae sulfated polysaccharide（SPA） on the proliferation of lung cancer and its possible mechanism.Methods: Using in vitro cell culture and animal model to observe the effects of SPA given by oral administration on tumor proliferation,immune function and the ability of IL-1, IL-2 secretion.Results:SPA at dose of 20, 40, 80 mg/kg significantly inhibits tumor growth with inhibitory rates of 35.27%(P<0.01), 4829%(P<0.001), 65.41% respectively. Significant increase in phagocytic function, increase in serun hemolycin level, delayed allergic reaction and secrection of IL-1，IL-2 were observed after SPA administration. No direct inhibitory effect on proliferation of A459 adenocarcinoma cell was observed in vitro.Conclusion: SPA inhibits the growth of Lewis lung cancer possibly by modulating immune function.
Objective: To explore the inhibitory effect of algae sulfated polysaccharide（SPA） on the proliferation of lung cancer and its possible mechanism.Methods: Using in vitro cell culture and animal model to observe the effects of SPA given by oral administration on tumor proliferation,immune function and the ability of IL-1, IL-2 secretion.Results:SPA at dose of 20, 40, 80 mg/kg significantly inhibits tumor growth with inhibitory rates of 35.27%(P<0.01), 4829%(P<0.001), 65.41% respectively. Significant increase in phagocytic function, increase in serun hemolycin level, delayed allergic reaction and secrection of IL-1，IL-2 were observed after SPA administration. No direct inhibitory effect on proliferation of A459 adenocarcinoma cell was observed in vitro.Conclusion: SPA inhibits the growth of Lewis lung cancer possibly by modulating immune function.
2003, 10(4):265-268.
DOI: 10.3872/j.issn.1007-385X.2003.4.008
Abstract:
Objective:To investigate the expression of AKT and PTEN protein and their relationship with clinic characteristics of esophageal carcinoma.Methods: Expression of AKT and PTEN protein was examined by Western Blot and immunohistochemical method in the esophageal carcinoma and normal esophageal (control) tissue of 42 patients.Results: In tumor specimen, expression of AKT protein was increased as compared with control tissue(P<0.01), while PTEN protein was reduced compared with control tissue(P<0.01). A negative correlation was observed between AKT and PTEN(r=-0.583，P<0.01). Protein level of AKT was higher in Ⅲb-Ⅳ stage patients with low differentiatition and lymph node metastasis than those with Ⅱ-Ⅲastage, high defferentiatition and no lymph node metastasis(P<0.01). However, PTEN protein level was entirely contrary. Both of them were not related with age, sex and size of tumor(P>0.05).Conclusions: The hyperexpression of AKT may play an important role in the initiation and development of human esophageal carcinoma, while PTEN inhibit this process.
Objective:To investigate the expression of AKT and PTEN protein and their relationship with clinic characteristics of esophageal carcinoma.Methods: Expression of AKT and PTEN protein was examined by Western Blot and immunohistochemical method in the esophageal carcinoma and normal esophageal (control) tissue of 42 patients.Results: In tumor specimen, expression of AKT protein was increased as compared with control tissue(P<0.01), while PTEN protein was reduced compared with control tissue(P<0.01). A negative correlation was observed between AKT and PTEN(r=-0.583，P<0.01). Protein level of AKT was higher in Ⅲb-Ⅳ stage patients with low differentiatition and lymph node metastasis than those with Ⅱ-Ⅲastage, high defferentiatition and no lymph node metastasis(P<0.01). However, PTEN protein level was entirely contrary. Both of them were not related with age, sex and size of tumor(P>0.05).Conclusions: The hyperexpression of AKT may play an important role in the initiation and development of human esophageal carcinoma, while PTEN inhibit this process.
2003, 10(4):269-273.
DOI: 10.3872/j.issn.1007-385X.2003.4.009
Abstract:
Objective: To explore biological characteristics of AFP gene-modified DC tumor vaccine in vitro. Methods: The recombinant adenovirus expression plasmid Ad-AFP which carries the full length cDNA of mice AFP was transfected into bone marrow-derived dendritic cell(BMDC), to construct AFP-DC Hepatocarcinoma tumor vaccine. The effectiveness of transfection was detected by electrochemiluminescence immunoassay. Surface molecules and phagocytosis of AFP-DC were detected by FACS. Mice T cell proliferation stimulated by AFP-DC were detected by 3H-TdR uptake assay. Cytotoxic CTL activity induced by AFP-DC in vitro was detected by 51Cr releasing assay. Results: AFP secreted by AFP-DC could be detected on surfaces of DCs and their supernatants after being transfected for 12 hours, which was suggested that the transfection was effective. B7 was obviously higher, MHC slightly higher and phagocytosis lower for AFP-DC compared with BMDC(P<005). Isogenotype T cell proliferation induced by DC-AFP were obviously higher than DC control group and LacZ-DC group(P<0.05). The cytotoxicity of CTL induced in vitro by AFP-DC to hepatoma Hepal-6 cells have specificity. Conclusion: Hepatocarcinoma associated antigen AFP could be used as a cut in point to gene therapy of hepatoma. The research provided experimental bases for immunotherapy of Hepatocarcinoma mediated by DC.
Objective: To explore biological characteristics of AFP gene-modified DC tumor vaccine in vitro. Methods: The recombinant adenovirus expression plasmid Ad-AFP which carries the full length cDNA of mice AFP was transfected into bone marrow-derived dendritic cell(BMDC), to construct AFP-DC Hepatocarcinoma tumor vaccine. The effectiveness of transfection was detected by electrochemiluminescence immunoassay. Surface molecules and phagocytosis of AFP-DC were detected by FACS. Mice T cell proliferation stimulated by AFP-DC were detected by 3H-TdR uptake assay. Cytotoxic CTL activity induced by AFP-DC in vitro was detected by 51Cr releasing assay. Results: AFP secreted by AFP-DC could be detected on surfaces of DCs and their supernatants after being transfected for 12 hours, which was suggested that the transfection was effective. B7 was obviously higher, MHC slightly higher and phagocytosis lower for AFP-DC compared with BMDC(P<005). Isogenotype T cell proliferation induced by DC-AFP were obviously higher than DC control group and LacZ-DC group(P<0.05). The cytotoxicity of CTL induced in vitro by AFP-DC to hepatoma Hepal-6 cells have specificity. Conclusion: Hepatocarcinoma associated antigen AFP could be used as a cut in point to gene therapy of hepatoma. The research provided experimental bases for immunotherapy of Hepatocarcinoma mediated by DC.
2003, 10(4):274-276.
DOI: 10.3872/j.issn.1007-385X.2003.4.010
Abstract:
Objective:To investigate the anti-tumor effect of recombinant human Endostatin (rhu-Endostatin)on the growth of mouse Lewis lung carcinoma cells, and to elucidate the dose-effect relationship and its possible mechanism. Methods:Lewis lung carcinoma cells were inoculated to mice (10 6-/ml). When trmor size reached about 100 mm3, the mice were randomly divided into low, medium and high dose groups with saline and CSA \[100 mg/（kg·d)\] as control. Rhu-Endostatin \[5,15, 30 mg/(kg·d)\] was injected to mouse once a day for 21days. At the 22 nd day, mice were executed, the tumor weights was calculated, and sections of brain, lung, liver, spleen and kidney was subjected to physiological analysis. Results: Area under curve in the endostatin-treated group was obviously less than that in tamor control group (P<0.01). Pathological study revealed that lavge areal necrosis arose in tumor and newborn capillaries around the tumor disappeared. Conclusion: The results revealed that rhu-Endostatin inhibited the growth, metastasis and angiogenesis of mouse Lewis lung carcinoma with the highest inhibition rate of 58.8%.
Objective:To investigate the anti-tumor effect of recombinant human Endostatin (rhu-Endostatin)on the growth of mouse Lewis lung carcinoma cells, and to elucidate the dose-effect relationship and its possible mechanism. Methods:Lewis lung carcinoma cells were inoculated to mice (10 6-/ml). When trmor size reached about 100 mm3, the mice were randomly divided into low, medium and high dose groups with saline and CSA \[100 mg/（kg·d)\] as control. Rhu-Endostatin \[5,15, 30 mg/(kg·d)\] was injected to mouse once a day for 21days. At the 22 nd day, mice were executed, the tumor weights was calculated, and sections of brain, lung, liver, spleen and kidney was subjected to physiological analysis. Results: Area under curve in the endostatin-treated group was obviously less than that in tamor control group (P<0.01). Pathological study revealed that lavge areal necrosis arose in tumor and newborn capillaries around the tumor disappeared. Conclusion: The results revealed that rhu-Endostatin inhibited the growth, metastasis and angiogenesis of mouse Lewis lung carcinoma with the highest inhibition rate of 58.8%.
2003, 10(4):277-279.
DOI: 10.3872/j.issn.1007-385X.2003.4.011
Abstract:
Objective: To evaluate the efficacy of granulocyte(-macrophage) colony stimulating factor［G(M)-CSF］ in the treatment of concomitant chemoradiotherapy-induced oral mucositis in locally advanced head and neck cancer patients.Metheds: Fifteen patients with locally advanced head and neck cancer was received concomitant chemoradiotherapy,while white blood cell count were less than 1.5×10 9/L with grade Ⅲ/Ⅳoral mucositis ,they were subcutaneously given G(M)-CSF at dose of 100-300 μg daily for 3-10 days.Results: After administration of G(M)-CSF,all of the patients had an augmantation of white blood cell count more than 5.0×10 9/L. Complete healing of oral mucositis occurred in 1 patient(CR), partial in 8 patients(PR),whereas 6 patients had no change and none was progressive,the objective response rate(CR+PR) was 60%.Conclusions: G(M)-CSF is proved effective for oral mucositis caused by concomitant chemoradiotherapy in locally advanced head and neck cancer patients.
Objective: To evaluate the efficacy of granulocyte(-macrophage) colony stimulating factor［G(M)-CSF］ in the treatment of concomitant chemoradiotherapy-induced oral mucositis in locally advanced head and neck cancer patients.Metheds: Fifteen patients with locally advanced head and neck cancer was received concomitant chemoradiotherapy,while white blood cell count were less than 1.5×10 9/L with grade Ⅲ/Ⅳoral mucositis ,they were subcutaneously given G(M)-CSF at dose of 100-300 μg daily for 3-10 days.Results: After administration of G(M)-CSF,all of the patients had an augmantation of white blood cell count more than 5.0×10 9/L. Complete healing of oral mucositis occurred in 1 patient(CR), partial in 8 patients(PR),whereas 6 patients had no change and none was progressive,the objective response rate(CR+PR) was 60%.Conclusions: G(M)-CSF is proved effective for oral mucositis caused by concomitant chemoradiotherapy in locally advanced head and neck cancer patients.
2003, 10(4):280-284.
DOI: 10.3872/j.issn.1007-385X.2003.4.012
Abstract:
Objective:To establish a sensitive and effective bioassay method for in vitro evaluation of biological activity of recombinant human neu epitope peptide 12. Methods:Mice were used in the test. By comparing results of antibody for an ELISA in different species of mouse, including dosage and production intervals of immunization and parameters, an in vitro bioassay protocol was formulated. Results:According to dose-response curve of recombinant human neu epitope peptide 12 on FVB transgenic mice(TgN MMTVneu 202 Mul，Jackson Lab.，USA), the optimal reaction time and dosage were determined. The results were accurate, and objective, and had good reproducibility, CV% is 6.7% (n=4); the percentage of positive mice were used for biological activity evaluation of recombinant human neu epitope peptide 12. Conclusion:The established method of using FVB transgenic mice to test the recombinant human neu epitope peptide 12 bioactivity can be used in routine control of the biological activity evaluation of recombinant human neu epitope peptide 12.
Objective:To establish a sensitive and effective bioassay method for in vitro evaluation of biological activity of recombinant human neu epitope peptide 12. Methods:Mice were used in the test. By comparing results of antibody for an ELISA in different species of mouse, including dosage and production intervals of immunization and parameters, an in vitro bioassay protocol was formulated. Results:According to dose-response curve of recombinant human neu epitope peptide 12 on FVB transgenic mice(TgN MMTVneu 202 Mul，Jackson Lab.，USA), the optimal reaction time and dosage were determined. The results were accurate, and objective, and had good reproducibility, CV% is 6.7% (n=4); the percentage of positive mice were used for biological activity evaluation of recombinant human neu epitope peptide 12. Conclusion:The established method of using FVB transgenic mice to test the recombinant human neu epitope peptide 12 bioactivity can be used in routine control of the biological activity evaluation of recombinant human neu epitope peptide 12.
2003, 10(4):285-288.
DOI: 10.3872/j.issn.1007-385X.2003.4.013
Abstract:
Objective: To investigate the expression of mdr-1 and mrp genes and observe the effects of arsenic trioxide (As2O3) on the gene expression.Methods: The doze of cytotoxicity and non-cytotoxicity of As2O3 was examined through MTT assay. The expressions of mdr-1 and mrp genes were studied by RT-PCR method.Results: The non-cytotoxic dose of As2O3 was 0.2 μmol/L and the low cytotoxic dose was 0.8 μmol/L to MCF-7/ADM cell line(P<0.05). Expression of mdr-1 and mrp genes was positive in MCF-7/ADM cells, and the expression of mdr-1 was stronger than the mrp gene, then the expression of mdr-1 and mrp genes was negative in the MCF-7/S cells; Arsenic trioxide could down-regulate the expression of mdr-1 and mrp genes in MCF-7/ADM and the lowcytotoxic dose of As2O3 had more strong effect than the non-cytotoxic dose of As2O3. Conclusions:The strong expressions of mdr-1 and mrp genes were responsible for the induced resistance of MCF-7/ADM cells to ADM; Arsenic trioxide reverses partly the multidrug resistance of the MCF-7/ADM cells with more kinds of biologic mechanisms.
Objective: To investigate the expression of mdr-1 and mrp genes and observe the effects of arsenic trioxide (As2O3) on the gene expression.Methods: The doze of cytotoxicity and non-cytotoxicity of As2O3 was examined through MTT assay. The expressions of mdr-1 and mrp genes were studied by RT-PCR method.Results: The non-cytotoxic dose of As2O3 was 0.2 μmol/L and the low cytotoxic dose was 0.8 μmol/L to MCF-7/ADM cell line(P<0.05). Expression of mdr-1 and mrp genes was positive in MCF-7/ADM cells, and the expression of mdr-1 was stronger than the mrp gene, then the expression of mdr-1 and mrp genes was negative in the MCF-7/S cells; Arsenic trioxide could down-regulate the expression of mdr-1 and mrp genes in MCF-7/ADM and the lowcytotoxic dose of As2O3 had more strong effect than the non-cytotoxic dose of As2O3. Conclusions:The strong expressions of mdr-1 and mrp genes were responsible for the induced resistance of MCF-7/ADM cells to ADM; Arsenic trioxide reverses partly the multidrug resistance of the MCF-7/ADM cells with more kinds of biologic mechanisms.
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Chinese Journal Of Cancer Biotheray ® 2025 All Rights Reserved
Supported by:Beijing E-Tiller Technology Development Co., Ltd.