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Volume 6,Issue 4,1999 Table of Contents
1999, 6(4):246-249.
DOI: 10.3872/j.issn.1007-385X.1999.4.002
Abstract:
Objective: RA538 is a differentiation-relating gene isolated from a human esophageal cancer cell line which is terminally differentiated induced by retinoic acid. In the present study, the functions of and-tumor of RA538 gene are investigated. Methods: The transfeution of RA538 gene, the effects of inhibition on tumor cells were observed. Results: The transfection of RA538 gene into human lung adenocarcinoma cell line (GLC-82) and colon carcinoma cell line (HCT) by recombined adenovirus results in a fairly high transfection efficiency, showing an obvious suppression to tumor growth (suppression rate: 77 .2 % and 77 . 9% respectively) and a reduction of tumor forming ability of the two cell lines in vivo. FCM.DNA fragmentation analysis and TUNEL domonstrate RA538 can induce apoptosis of tumor cells. Western blot analysis shows that RA538 downregulated c-myc gene expression. Conclusion: The results suggest that RA538 could be a new tumor suppresser gene in tumor gene therapy.
Objective: RA538 is a differentiation-relating gene isolated from a human esophageal cancer cell line which is terminally differentiated induced by retinoic acid. In the present study, the functions of and-tumor of RA538 gene are investigated. Methods: The transfeution of RA538 gene, the effects of inhibition on tumor cells were observed. Results: The transfection of RA538 gene into human lung adenocarcinoma cell line (GLC-82) and colon carcinoma cell line (HCT) by recombined adenovirus results in a fairly high transfection efficiency, showing an obvious suppression to tumor growth (suppression rate: 77 .2 % and 77 . 9% respectively) and a reduction of tumor forming ability of the two cell lines in vivo. FCM.DNA fragmentation analysis and TUNEL domonstrate RA538 can induce apoptosis of tumor cells. Western blot analysis shows that RA538 downregulated c-myc gene expression. Conclusion: The results suggest that RA538 could be a new tumor suppresser gene in tumor gene therapy.
1999, 6(4):252-256.
DOI: 10.3872/j.issn.1007-385X.1999.4.004
Abstract:
目的:为进一步研究其结构与功能的关系.方法:利用MSI公司的Insight Ⅱ分子模拟软件,参照TNF-α的三级结构信息文件,对TRAIL分子胞外区的R117到G281共165个氨基酸残基进行了同源性模建;并利用Profile-3D程序中的Inverse Fold-ing方法对模建结果进行可靠性分析.结果:模建出的TRAIL分子共含10个β-片层结构,且这些β-片层均对应于TNF-α中相应的β-片层区.这与同一家族的分子在结构保守区,特别是形成二级结构的保守区中序列组成变化不大的理论相吻合.而且验证模建结果的结果可靠性积分值为55.80.结论:模建结果基本正确,为TRALL的结构与功能研究提供了基础.
目的:为进一步研究其结构与功能的关系.方法:利用MSI公司的Insight Ⅱ分子模拟软件,参照TNF-α的三级结构信息文件,对TRAIL分子胞外区的R117到G281共165个氨基酸残基进行了同源性模建;并利用Profile-3D程序中的Inverse Fold-ing方法对模建结果进行可靠性分析.结果:模建出的TRAIL分子共含10个β-片层结构,且这些β-片层均对应于TNF-α中相应的β-片层区.这与同一家族的分子在结构保守区,特别是形成二级结构的保守区中序列组成变化不大的理论相吻合.而且验证模建结果的结果可靠性积分值为55.80.结论:模建结果基本正确,为TRALL的结构与功能研究提供了基础.
1999, 6(4):257-260.
DOI: 10.3872/j.issn.1007-385X.1999.4.005
Abstract:
目的:肿瘤细胞表达MHCⅠ类分子是激发肿瘤抗原特异性CTL进行肿瘤免疫治疗的关键,肿瘤细胞HLAⅠ类分子表达异常是肿瘤逃脱免疫监视的重要机制.我们探讨了卵巢癌细胞HLAⅠ类分子表达异常的分子基础.方法:本文以West-ern blot、免疫组化和流式细胞术检测卵巢癌细胞HLA Ⅰ类分子的表达,以RT-PCR检测TAP,IMP基因的表达,探讨肿瘤细胞HLA Ⅰ类分子表达异常的分子基础.结果:卵巢癌中HLA Ⅰ类分子表达异常相当普遍(5/8),并涉及抗原加工相关基因TAP,LMP基因表达异常.25℃培养肿瘤细胞可部分诱导Ⅰ类分子的表达;结论:卵巢癌HLA Ⅰ类分子表达异常与其Ⅰ类抗原加工途径异常有关.
目的:肿瘤细胞表达MHCⅠ类分子是激发肿瘤抗原特异性CTL进行肿瘤免疫治疗的关键,肿瘤细胞HLAⅠ类分子表达异常是肿瘤逃脱免疫监视的重要机制.我们探讨了卵巢癌细胞HLAⅠ类分子表达异常的分子基础.方法:本文以West-ern blot、免疫组化和流式细胞术检测卵巢癌细胞HLA Ⅰ类分子的表达,以RT-PCR检测TAP,IMP基因的表达,探讨肿瘤细胞HLA Ⅰ类分子表达异常的分子基础.结果:卵巢癌中HLA Ⅰ类分子表达异常相当普遍(5/8),并涉及抗原加工相关基因TAP,LMP基因表达异常.25℃培养肿瘤细胞可部分诱导Ⅰ类分子的表达;结论:卵巢癌HLA Ⅰ类分子表达异常与其Ⅰ类抗原加工途径异常有关.
1999, 6(4):261-264.
DOI: 10.3872/j.issn.1007-385X.1999.4.006
Abstract:
Objective: To investigate the killing effects of HSV-tk/GCV system on murine liver cancer cells in vitro. Methods: HSV-tk gene was cloned into retroviral vector (pLNCTK) by recombinant DNA technology. After packaging with PA317 cell line, murine liver cancer cell line MM45T.Li was infected by the recombinant retrovirus. The positive clones were obtained after G418 selection and it was termed MM45T. Li/TK. The integration and expression of tk gene in MM45T. Li/TK cells were identified by PCR and RT-PCR. The killing effects of GCV on TK cell alone or a mixture of TK and TK~(-) cells in different ratio were observed. Results: (1) PCR and RT-PCR analysis confirmed integration of HSV-tk gene in positive clone, and expression of HSV-tk gene at mRNA level. (2) There was no significant difference in cell proliferation or morphology between the MM45T. Li/TK and MM45T. Li. (3) The cytotoxicity of GCV in MM45T. Li/TK cells was 1 000 fold higher sensitive than that in parental MM45T.U cells. (4) When MM45T.Li/TK cells were mixed with parental MM45T. Li cells at a ratio of 25:75, significant bystander effect was observed in vitro after they were treated with nontoxic GCV. Conclusions: These results suggested that murine liver cancer cells were sensitive to HSV-tk/GCV system and had significant bystander effects.
Objective: To investigate the killing effects of HSV-tk/GCV system on murine liver cancer cells in vitro. Methods: HSV-tk gene was cloned into retroviral vector (pLNCTK) by recombinant DNA technology. After packaging with PA317 cell line, murine liver cancer cell line MM45T.Li was infected by the recombinant retrovirus. The positive clones were obtained after G418 selection and it was termed MM45T. Li/TK. The integration and expression of tk gene in MM45T. Li/TK cells were identified by PCR and RT-PCR. The killing effects of GCV on TK cell alone or a mixture of TK and TK~(-) cells in different ratio were observed. Results: (1) PCR and RT-PCR analysis confirmed integration of HSV-tk gene in positive clone, and expression of HSV-tk gene at mRNA level. (2) There was no significant difference in cell proliferation or morphology between the MM45T. Li/TK and MM45T. Li. (3) The cytotoxicity of GCV in MM45T. Li/TK cells was 1 000 fold higher sensitive than that in parental MM45T.U cells. (4) When MM45T.Li/TK cells were mixed with parental MM45T. Li cells at a ratio of 25:75, significant bystander effect was observed in vitro after they were treated with nontoxic GCV. Conclusions: These results suggested that murine liver cancer cells were sensitive to HSV-tk/GCV system and had significant bystander effects.
1999, 6(4):265-267.
DOI: 10.3872/j.issn.1007-385X.1999.4.007
Abstract:
Objective: To prepare the conjugate of supcrantigen (SAg) staphylococcal enterotoxin A (SEA) and monoclonal antibody (McAb) against human hepatocellular carcinoma HAbl8 F(ab' )_(2) fragment and to investigate the anti-human hepatoma effect of peripheral blood mononuclear cells (PBMC) targeted by HAbl8 F(ab' )i-SEA. Methods: McAb HAbl8 was extracted and its F(ab' )_(2) fragment was prepared with papain; the conjugate HAblS F(ab' )_(2)-SEA was prepared with N-succinimidyl-3-(2-pyridyldithio) propionate (SPDP); eveny collected peak after purification was identified with gel chromatography; the activity of antibody in the conjugate was identified with immunohistocheinical ABC method; the anti-hepatoma effect of PBMC targeted by HAbl8 F(ab' )_(2)-SEA was observed with MTT method. Results: The conjugate HAbl8 F(ab' )_(2)-SEA was prepared successfully and it had obvious effect of targeting PBMC to kill hepatoma cells, and this effect is correlated positively with the dose of HAbl8 F(ab')_(2)-SEA. Control groups had no such effect. Conclusion: Targeting therapy of hepatoma with McAb-SAg conjugate might be a kind of hopeful model of hepatoma im-munotherapy.
Objective: To prepare the conjugate of supcrantigen (SAg) staphylococcal enterotoxin A (SEA) and monoclonal antibody (McAb) against human hepatocellular carcinoma HAbl8 F(ab' )_(2) fragment and to investigate the anti-human hepatoma effect of peripheral blood mononuclear cells (PBMC) targeted by HAbl8 F(ab' )i-SEA. Methods: McAb HAbl8 was extracted and its F(ab' )_(2) fragment was prepared with papain; the conjugate HAblS F(ab' )_(2)-SEA was prepared with N-succinimidyl-3-(2-pyridyldithio) propionate (SPDP); eveny collected peak after purification was identified with gel chromatography; the activity of antibody in the conjugate was identified with immunohistocheinical ABC method; the anti-hepatoma effect of PBMC targeted by HAbl8 F(ab' )_(2)-SEA was observed with MTT method. Results: The conjugate HAbl8 F(ab' )_(2)-SEA was prepared successfully and it had obvious effect of targeting PBMC to kill hepatoma cells, and this effect is correlated positively with the dose of HAbl8 F(ab')_(2)-SEA. Control groups had no such effect. Conclusion: Targeting therapy of hepatoma with McAb-SAg conjugate might be a kind of hopeful model of hepatoma im-munotherapy.
1999, 6(4):268-272.
DOI: 10.3872/j.issn.1007-385X.1999.4.008
Abstract:
目的:探讨FasL基因转染对肿瘤细胞化疗敏感性的调节效应,方法:LjpofectAMINE介导建立FasL基因修饰的乳腺癌细胞系MCF-7(?)FL,MTT法检测化疗药物对转染细胞的杀伤效应,半定量RT-PCR分析化疗药物作用前后转染细胞Fas mRNA表达水平变化,结果:经C418筛选,RT-PCR和免疫组化鉴定,建立FasL稳定表达MCF-7/FL,ADM在0.625～2.5μg′ml之间.MTX在3～6μg′ml.CDDP在1.25～10μg ml间对MCF-7FL的杀伤效应均明显高于MCF-7和转染空载体的MCF-7Vt而F(ab’)_2-APO-LMcAb可部分抑制这—增强效应,半定量RT-PCR显示上述化疗药物作用后MCF-7/FL Fas mRN水平表达显著增强,结论:外源FasL基因导入可上调肿瘤细胞对多种化疗药物的敏感性,其机制可能与化疗药物上调Fas表达从而增强瘤细胞FasL-Fas凋亡通路效应有关
目的:探讨FasL基因转染对肿瘤细胞化疗敏感性的调节效应,方法:LjpofectAMINE介导建立FasL基因修饰的乳腺癌细胞系MCF-7(?)FL,MTT法检测化疗药物对转染细胞的杀伤效应,半定量RT-PCR分析化疗药物作用前后转染细胞Fas mRNA表达水平变化,结果:经C418筛选,RT-PCR和免疫组化鉴定,建立FasL稳定表达MCF-7/FL,ADM在0.625～2.5μg′ml之间.MTX在3～6μg′ml.CDDP在1.25～10μg ml间对MCF-7FL的杀伤效应均明显高于MCF-7和转染空载体的MCF-7Vt而F(ab’)_2-APO-LMcAb可部分抑制这—增强效应,半定量RT-PCR显示上述化疗药物作用后MCF-7/FL Fas mRN水平表达显著增强,结论:外源FasL基因导入可上调肿瘤细胞对多种化疗药物的敏感性,其机制可能与化疗药物上调Fas表达从而增强瘤细胞FasL-Fas凋亡通路效应有关
1999, 6(4):273-276.
DOI: 10.3872/j.issn.1007-385X.1999.4.009
Abstract:
Objective: To select suitable conditions for prokaryotic expression and purification of rhIL-17. Methods: rhIL-17 was expressed in E. coli host under heat induction. After compared among the expression amounts in different media under different heat induction time, the most suitable conditions was selected. The target protein was present in the form of inclusion body. The precipitate of inclusion was obtained and purified after 6M guanidine solublization or 2% SDS solublization. Results: Either protocol could yield rhIL-17 with high purity and stable activity. The SDS solublization mehthod gives rise to much more higher productivity than the guanidine solublization method. Conclusion: rhIL-17 were expression in E. coli system and purified to homogenicity by SDS solublization methods with high productivity.
Objective: To select suitable conditions for prokaryotic expression and purification of rhIL-17. Methods: rhIL-17 was expressed in E. coli host under heat induction. After compared among the expression amounts in different media under different heat induction time, the most suitable conditions was selected. The target protein was present in the form of inclusion body. The precipitate of inclusion was obtained and purified after 6M guanidine solublization or 2% SDS solublization. Results: Either protocol could yield rhIL-17 with high purity and stable activity. The SDS solublization mehthod gives rise to much more higher productivity than the guanidine solublization method. Conclusion: rhIL-17 were expression in E. coli system and purified to homogenicity by SDS solublization methods with high productivity.
1999, 6(4):280-283.
DOI: 10.3872/j.issn.1007-385X.1999.4.011
Abstract:
Objective: To investigate the efficiency of treatment with angiostatin on melanoma. Methods: Angiostatin was purified through affinity chromatography from human plasminogen fragments obtained by digesting human plasminogen with elastase. Results: The result of experiment in vitro showed that the purified angiostatin could significantly inhibit the proliferation of bovine aortic endothelial cells stimulated by bFGF. Systematic administration of angiostatin at does of 0.6 mg/kg d for 14 days, the tumor weight reduced about 77 % ( P < 0.05) . We established the melanoma metastasis model by injection of B16 cells through mouse tail vein. Under the same treatment for 18 days, the melanoma lung metastasis reduced about 65 % ( P < 0.05) . Conclusion: Our results supply the experimental evidence for the application of angiostatin in melanoma therapy.
Objective: To investigate the efficiency of treatment with angiostatin on melanoma. Methods: Angiostatin was purified through affinity chromatography from human plasminogen fragments obtained by digesting human plasminogen with elastase. Results: The result of experiment in vitro showed that the purified angiostatin could significantly inhibit the proliferation of bovine aortic endothelial cells stimulated by bFGF. Systematic administration of angiostatin at does of 0.6 mg/kg d for 14 days, the tumor weight reduced about 77 % ( P < 0.05) . We established the melanoma metastasis model by injection of B16 cells through mouse tail vein. Under the same treatment for 18 days, the melanoma lung metastasis reduced about 65 % ( P < 0.05) . Conclusion: Our results supply the experimental evidence for the application of angiostatin in melanoma therapy.
1999, 6(4):284-287.
DOI: 10.3872/j.issn.1007-385X.1999.4.012
Abstract:
Objective: Study on the growth character of B16 melanoma cell which can express angiostatin. Methods: Angiostatin gene was constructed from human plasminogen cDNA by deletion mutation. A B16 melanoma cell clone named BAG28 which stably expresses angiostatin was established by introducing gene into it. Results: BAG28 in vitro had no changes in proliferation rate and the ability of clone formation in soft agar. Study in vitro showed that the tumor weight had reduced about 87% ( P < 0. 01 ) 26 days after inoculation in mouse. Conclusion: The growth of B16 melanoma cells expressing angiostain was significandy inhibited in vivo.
Objective: Study on the growth character of B16 melanoma cell which can express angiostatin. Methods: Angiostatin gene was constructed from human plasminogen cDNA by deletion mutation. A B16 melanoma cell clone named BAG28 which stably expresses angiostatin was established by introducing gene into it. Results: BAG28 in vitro had no changes in proliferation rate and the ability of clone formation in soft agar. Study in vitro showed that the tumor weight had reduced about 87% ( P < 0. 01 ) 26 days after inoculation in mouse. Conclusion: The growth of B16 melanoma cells expressing angiostain was significandy inhibited in vivo.
10 Isolation and Sequencing the Differential Gene Fragments Expressed in Human Stomach Cancer Tissue
1999, 6(4):288-291.
DOI: 10.3872/j.issn.1007-385X.1999.4.013
Abstract:
Objective: Identification of the genes specially expressed in tumor cell but not in normal cell is important for understanding the molecular mechanisms of carcinogencsis. This study will focus on identification of differentially expressed gene fragments in human stomach cancer. Methods: By using the new developing mRNA differential display (DD) technique, genes fragments differentially expressed in stomach cancer tissues from a patient and the adjacent normal tissues beyond the tumor mass were studied. Results: Two differentially displayed complementary DNA fragments from stomach cancer tissues, scgl and scg2 (stomach cancer-associated gene, scg), cofirmed by Northern Blot, were cloned and sequenced. The nucleotide length of scgl is 194 base pairs and that of scg2 is 343 base pairs. After searching against GenBank databases by BLASTN, neither scgl nor scg2 had significant homological gene sequences with the known genes. Conclusion: These results suggested scgl and scg2 might be complementary DNA fragments of novel genes expressed in stomach cancer tissues, but not in normal tissues and may play a role in the occurrence and development of stomach cancer. Further characterization of full-length of these two complementary DNA fragments will be continued.
Objective: Identification of the genes specially expressed in tumor cell but not in normal cell is important for understanding the molecular mechanisms of carcinogencsis. This study will focus on identification of differentially expressed gene fragments in human stomach cancer. Methods: By using the new developing mRNA differential display (DD) technique, genes fragments differentially expressed in stomach cancer tissues from a patient and the adjacent normal tissues beyond the tumor mass were studied. Results: Two differentially displayed complementary DNA fragments from stomach cancer tissues, scgl and scg2 (stomach cancer-associated gene, scg), cofirmed by Northern Blot, were cloned and sequenced. The nucleotide length of scgl is 194 base pairs and that of scg2 is 343 base pairs. After searching against GenBank databases by BLASTN, neither scgl nor scg2 had significant homological gene sequences with the known genes. Conclusion: These results suggested scgl and scg2 might be complementary DNA fragments of novel genes expressed in stomach cancer tissues, but not in normal tissues and may play a role in the occurrence and development of stomach cancer. Further characterization of full-length of these two complementary DNA fragments will be continued.
1999, 6(4):292-294.
DOI: 10.3872/j.issn.1007-385X.1999.4.014
Abstract:
Objective: To investigate estrogen receptor (ER) and progesterone receptor (PR) in the tumor derived from non-target organ (primary bronchogenic carcinoma), and correlation with the tumor. Methods: According to WHO histo-logical classification of lung tumors, 146 resected specimens of lung canrer were examined microscopically; ER and PR were detected on paraffin-embedded tissue sections using immunohistochemical staining. Results: 58.9% of the cases were positive for ER, 69. 1 % for PR,and 46.6% positive for both. There was a significant correlation between ER and PR positive percentage and degrees of histological differentiation in lung cancer, while ER and PR percentage appears to have no relationship with histological type, tumor size, age and sex of the patients. Conclusion: It is demonstrated that ER and PR are present in non-small cell lung cancer. These observation may provide a basis for adjuvant hormonal therapy in selected lung cancer patients.
Objective: To investigate estrogen receptor (ER) and progesterone receptor (PR) in the tumor derived from non-target organ (primary bronchogenic carcinoma), and correlation with the tumor. Methods: According to WHO histo-logical classification of lung tumors, 146 resected specimens of lung canrer were examined microscopically; ER and PR were detected on paraffin-embedded tissue sections using immunohistochemical staining. Results: 58.9% of the cases were positive for ER, 69. 1 % for PR,and 46.6% positive for both. There was a significant correlation between ER and PR positive percentage and degrees of histological differentiation in lung cancer, while ER and PR percentage appears to have no relationship with histological type, tumor size, age and sex of the patients. Conclusion: It is demonstrated that ER and PR are present in non-small cell lung cancer. These observation may provide a basis for adjuvant hormonal therapy in selected lung cancer patients.
1999, 6(4):302-304.
DOI: 10.3872/j.issn.1007-385X.1999.4.017
Abstract:
Objective: To study the therapeutic effect of CEA recombinant vaccinia virus on CEA positive tumor. Methords: The CEA positive cell model of murine Hepa liver cancer was constructed. Then, 40 mice, which were divided into four groups, were injected subcutaneously with CEA positive or CEA negative Hepa tumor cells respectively, and followed by subcutaneous vaccination of wild-type vaccinia virus (W-VV ) or CEA-rV for three times at 14-day interval . The animals responses were observed and the subcutaneous tumors were measured weekly after tumor cells injection. Results: Subcutaneous tumors were observed in all mice. Three control groups tumors grew relatively fast, no statistic significance between these groups were obtained ( P > 0.05), whereas the tumors in group four, which were injected with Hepa-CEA~( ) tumor cells and CEA-rV , grew slowly and the tumor mass was smaller. Comparison with the three control groups, the difference was significant in statistics ( P < 0.01). During the whole testing period, no toxic or side-effects were seen in all animals. Conclusion: The results showed that CEA-rV had well therapeutic effect on CEA positive tumors through inducing the body's immune system to produce CEA specific immune responses.
Objective: To study the therapeutic effect of CEA recombinant vaccinia virus on CEA positive tumor. Methords: The CEA positive cell model of murine Hepa liver cancer was constructed. Then, 40 mice, which were divided into four groups, were injected subcutaneously with CEA positive or CEA negative Hepa tumor cells respectively, and followed by subcutaneous vaccination of wild-type vaccinia virus (W-VV ) or CEA-rV for three times at 14-day interval . The animals responses were observed and the subcutaneous tumors were measured weekly after tumor cells injection. Results: Subcutaneous tumors were observed in all mice. Three control groups tumors grew relatively fast, no statistic significance between these groups were obtained ( P > 0.05), whereas the tumors in group four, which were injected with Hepa-CEA~( ) tumor cells and CEA-rV , grew slowly and the tumor mass was smaller. Comparison with the three control groups, the difference was significant in statistics ( P < 0.01). During the whole testing period, no toxic or side-effects were seen in all animals. Conclusion: The results showed that CEA-rV had well therapeutic effect on CEA positive tumors through inducing the body's immune system to produce CEA specific immune responses.
1999, 6(4):305-309.
DOI: 10.3872/j.issn.1007-385X.1999.4.018
Abstract:
目的:c-jun反义核酸消除人体卵巢癌细胞抗药性探讨.方法:采用c-jun反义核酸处理抗药型人体卵巢癌细胞,观察c-jun,γ-GCS以及GSH在两种细胞内的表达水平.结果:c-jun反义核酸可抑制c-jun基因的表达并降低谷胱苷肽合成的关键酶γ-GCS的mRNA表达量,使抗药型细胞内GSH含量降低大约75%.ATT分析结果也表明,经c-jun反义核酸处理后,抗药型细胞对顺铂的IC50从40μmol/L降低到1.0μmol/L,对敏感型细胞无明显影响（0.2μmol/L）.结论:c-jun反义核酸可特异地抑制抗药型细胞内c-jun基因的表达并间接抑制γ-GCS的表达,最终抑制GSH的合成,从而消除卵巢癌细胞的抗药性.
目的:c-jun反义核酸消除人体卵巢癌细胞抗药性探讨.方法:采用c-jun反义核酸处理抗药型人体卵巢癌细胞,观察c-jun,γ-GCS以及GSH在两种细胞内的表达水平.结果:c-jun反义核酸可抑制c-jun基因的表达并降低谷胱苷肽合成的关键酶γ-GCS的mRNA表达量,使抗药型细胞内GSH含量降低大约75%.ATT分析结果也表明,经c-jun反义核酸处理后,抗药型细胞对顺铂的IC50从40μmol/L降低到1.0μmol/L,对敏感型细胞无明显影响（0.2μmol/L）.结论:c-jun反义核酸可特异地抑制抗药型细胞内c-jun基因的表达并间接抑制γ-GCS的表达,最终抑制GSH的合成,从而消除卵巢癌细胞的抗药性.
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- 《中国肿瘤生物治疗杂志》
- 1994年创刊
- 主办单位：Chinese Society of Immunology, Chinese Anti-cancer Association
- 邮编：200433
- 电话：021-81871002-22
- 电子邮箱：cjcb@biother.cn
- 网址:http://www.biother.cn
- 刊号：ISSN 1007-385X
- CN 31-1725/R
- 国内定价： ￥20元/册
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Supported by:Beijing E-Tiller Technology Development Co., Ltd.