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Volume 5,Issue 1,1998 Table of Contents
1998, 5(1):1-2.
DOI: 10.3872/j.issn.1007-385X.1998.1.001
Abstract:
Egr-1 is a radiation-inducible transcription factor. It was demonstrated that the regulatory sequence in 5' flanking region of Egr-1 gene could confer the radiation inducibility upon a tumoricidal gene to which it was linked, and was consequently used in experiments on the gene-radiotherapy to tumor. As a first step to test the possibility, we have isolated the 445 bp-long regulatory sequence of Egr-1 gene from BALB/c mouse gcnomic DNA with PCR method. Sequence analysis confirmed that nucleotide sequence of this cloned fragment was identical with one reported previously with only one base difference in A to G substitution at residue - 392, and had six CC( A T)6GG domains which were essential to the radiation-inducible property of Egr-1 gene. This fragment then was inserted into the Mlu I-Bgl II site of pGL3, a reporter vector containing luciferase gene. The constructs were used to transfect mouse malignant melanoma cells (B16) to characterize the regulatory function of this CC ( A T)_(6)GG-rich sequence after exposure to r-radiation by a ~(60) Co source. The results indicate that the activity of luciferase in transfectant increases by 138% as compared with control levels, demonstrating that r-radiation inducibility of gene expression can be conferred by the regulatory sequence.
Egr-1 is a radiation-inducible transcription factor. It was demonstrated that the regulatory sequence in 5' flanking region of Egr-1 gene could confer the radiation inducibility upon a tumoricidal gene to which it was linked, and was consequently used in experiments on the gene-radiotherapy to tumor. As a first step to test the possibility, we have isolated the 445 bp-long regulatory sequence of Egr-1 gene from BALB/c mouse gcnomic DNA with PCR method. Sequence analysis confirmed that nucleotide sequence of this cloned fragment was identical with one reported previously with only one base difference in A to G substitution at residue - 392, and had six CC( A T)6GG domains which were essential to the radiation-inducible property of Egr-1 gene. This fragment then was inserted into the Mlu I-Bgl II site of pGL3, a reporter vector containing luciferase gene. The constructs were used to transfect mouse malignant melanoma cells (B16) to characterize the regulatory function of this CC ( A T)_(6)GG-rich sequence after exposure to r-radiation by a ~(60) Co source. The results indicate that the activity of luciferase in transfectant increases by 138% as compared with control levels, demonstrating that r-radiation inducibility of gene expression can be conferred by the regulatory sequence.
Wu Weizhong
,
Liu Kangda
,
Tang Zhaoyou
,
Tang Xiaolei
,
Wu Housheng
,
Hu Xinmei
,
Xie Qian
,
Gao Yanqin
1998, 5(1):5-8.
DOI: 10.3872/j.issn.1007-385X.1998.1.003
Abstract:
研究不同热休克条件对H22小鼠肝癌细胞的HSP70mRNA及蛋白表达的影响,以期获得最佳诱导条件.分别用MTT、RT-PCR、免疫荧光和FCM检测等方法观察不同热休克条件对鼠H22细胞的生存率、胞内HSP70mRNA转录水平及胞膜HSP70蛋白表达水平的改变.结果表明,H22细胞经轻度热休克(42～43℃),细胞生存率无影响,而中重度热休克(44～45℃)则随休克时间的延长,细胞生存率明显下降;42℃热休克初期(0.5～4小时)胞内HSP70mRNA水平低于对照组,休克后期(8～12小时)mRNA水平有所恢复并逐渐增高;不同时间热休克组H22细胞胞膜HSP70表达均较对照组显著增高(P
研究不同热休克条件对H22小鼠肝癌细胞的HSP70mRNA及蛋白表达的影响,以期获得最佳诱导条件.分别用MTT、RT-PCR、免疫荧光和FCM检测等方法观察不同热休克条件对鼠H22细胞的生存率、胞内HSP70mRNA转录水平及胞膜HSP70蛋白表达水平的改变.结果表明,H22细胞经轻度热休克(42～43℃),细胞生存率无影响,而中重度热休克(44～45℃)则随休克时间的延长,细胞生存率明显下降;42℃热休克初期(0.5～4小时)胞内HSP70mRNA水平低于对照组,休克后期(8～12小时)mRNA水平有所恢复并逐渐增高;不同时间热休克组H22细胞胞膜HSP70表达均较对照组显著增高(P
1998, 5(1):9-12.
DOI: 10.3872/j.issn.1007-385X.1998.1.004
Abstract:
p16 gene was a tumor supressor gene found recently. The p16 protein is a negative regulator of cell proliferation . Loss of normal p16 function is associated with the development of neoplasms. To detect antitumorigenic effect of p16 on human lung adenocarcinoma cells, we cloned a p16 cDNA into the pcDNA3 vector at the sites of BamHl and Xho I to gain a p16 gene recombinant expression vector plasmid. We then transferred the p16 gene recombinant plasmid into human lung adenocarcinoma cell line (NCI-H460) by electroporation method. After G418 selection we assessed cell growth properties and cell cycle pattern by flow cytometry to G418-resistant clones of NCI-H460-pl6 and NCI-H460-vect respectively. The results show that human p16 gene could suppress the phenotype of NCI-H460 cell line and p16 gene therapy plays a positive role in human lung adenocarcinoma treatment.
p16 gene was a tumor supressor gene found recently. The p16 protein is a negative regulator of cell proliferation . Loss of normal p16 function is associated with the development of neoplasms. To detect antitumorigenic effect of p16 on human lung adenocarcinoma cells, we cloned a p16 cDNA into the pcDNA3 vector at the sites of BamHl and Xho I to gain a p16 gene recombinant expression vector plasmid. We then transferred the p16 gene recombinant plasmid into human lung adenocarcinoma cell line (NCI-H460) by electroporation method. After G418 selection we assessed cell growth properties and cell cycle pattern by flow cytometry to G418-resistant clones of NCI-H460-pl6 and NCI-H460-vect respectively. The results show that human p16 gene could suppress the phenotype of NCI-H460 cell line and p16 gene therapy plays a positive role in human lung adenocarcinoma treatment.
1998, 5(1):13-15.
DOI: 10.3872/j.issn.1007-385X.1998.1.005
Abstract:
Interleukin-17 (IL-17) is a newly found cytokine secreted by activated T lymphocytes. From preliminary study, IL-17 was found to play a role in the relationship between T lymphocytes and hematopoiesis, but many of its characteristics remain unknown up to now. To investigate its biological functions and related mechanisms, we cloned the complete coding region of human IL-17(hIL-17) from activated human peripheral blood mononuclear cells (PBMC) by RT-PCR and constructed an integrative vector pLCM182-hIL-17 for cloning, expressing and sequencing the hIL-17 gene. By DNA sequencing, the cloned hIL-17 is identical to the reptorted, and with temperature inducing, the hEL-17 was highly expressed in E. coli up to 30% of bacterial protein. The expressed hIL-17 protein could stimulate primary human fibrob-lasts to secrete IL-6 and GM-CSF after initial purification. This results indicate that the expressed hIL-17 has biological activity.
Interleukin-17 (IL-17) is a newly found cytokine secreted by activated T lymphocytes. From preliminary study, IL-17 was found to play a role in the relationship between T lymphocytes and hematopoiesis, but many of its characteristics remain unknown up to now. To investigate its biological functions and related mechanisms, we cloned the complete coding region of human IL-17(hIL-17) from activated human peripheral blood mononuclear cells (PBMC) by RT-PCR and constructed an integrative vector pLCM182-hIL-17 for cloning, expressing and sequencing the hIL-17 gene. By DNA sequencing, the cloned hIL-17 is identical to the reptorted, and with temperature inducing, the hEL-17 was highly expressed in E. coli up to 30% of bacterial protein. The expressed hIL-17 protein could stimulate primary human fibrob-lasts to secrete IL-6 and GM-CSF after initial purification. This results indicate that the expressed hIL-17 has biological activity.
1998, 5(1):16-19.
DOI: 10.3872/j.issn.1007-385X.1998.1.006
Abstract:
Egr-1 is a radiation-inducible transcription factor. It was demonstrated that the regulatory sequence in 5' flanking region of Egr-1 gene could confer the radiation inducibility upon a tumoricidal gene to which it was linked, and was consequently used in experiments on the gene-radiotherapy to tumor. As a first step to test the possibility, we have isolated the 445 bp-long regulatory sequence of Egr-1 gene from BALB/c mouse gcnomic DNA with PCR method. Sequence analysis confirmed that nucleotide sequence of this cloned fragment was identical with one reported previously with only one base difference in A to G substitution at residue - 392, and had six CC( A T)6GG domains which were essential to the radiation-inducible property of Egr-1 gene. This fragment then was inserted into the Mlu I-Bgl II site of pGL3, a reporter vector containing luciferase gene. The constructs were used to transfect mouse malignant melanoma cells (B16) to characterize the regulatory function of this CC ( A T)_(6)GG-rich sequence after exposure to r-radiation by a ~(60) Co source. The results indicate that the activity of luciferase in transfectant increases by 138% as compared with control levels, demonstrating that r-radiation inducibility of gene expression can be conferred by the regulatory sequence.
Egr-1 is a radiation-inducible transcription factor. It was demonstrated that the regulatory sequence in 5' flanking region of Egr-1 gene could confer the radiation inducibility upon a tumoricidal gene to which it was linked, and was consequently used in experiments on the gene-radiotherapy to tumor. As a first step to test the possibility, we have isolated the 445 bp-long regulatory sequence of Egr-1 gene from BALB/c mouse gcnomic DNA with PCR method. Sequence analysis confirmed that nucleotide sequence of this cloned fragment was identical with one reported previously with only one base difference in A to G substitution at residue - 392, and had six CC( A T)6GG domains which were essential to the radiation-inducible property of Egr-1 gene. This fragment then was inserted into the Mlu I-Bgl II site of pGL3, a reporter vector containing luciferase gene. The constructs were used to transfect mouse malignant melanoma cells (B16) to characterize the regulatory function of this CC ( A T)_(6)GG-rich sequence after exposure to r-radiation by a ~(60) Co source. The results indicate that the activity of luciferase in transfectant increases by 138% as compared with control levels, demonstrating that r-radiation inducibility of gene expression can be conferred by the regulatory sequence.
1998, 5(1):20-23.
DOI: 10.3872/j.issn.1007-385X.1998.1.007
Abstract:
In order to study the bladder carcinoma cell growth suppression by introduction of foreign retinoblastoma (Rb) gene and explore a gene therapy approach for bladder cancer, a replication-deficient adenovirus vector encoding a wild-type Rb, AdCMVRb, was constructed and transfected into the cultured human bladder carcinoma cell line EJ. The efficiency of gene transfection and expression was detected by immunochemical staining, Western blotting and polymerase chain reaction. The role of Rb in suppressing EJ growth was observed by cell-counting, [3H]thymidine incorporation and flow cytometry. The results showed that wild-type Rb gene could be transfected effectively into cultured EJ with Ad-CMVRb and could arrest the cells at GO/Gl phases of the cell cycle, leading to inhibition of DNA synthesis. The results demonstrated the potential of adenovirus-mediated Rb gene therapy for bladder cancer.
In order to study the bladder carcinoma cell growth suppression by introduction of foreign retinoblastoma (Rb) gene and explore a gene therapy approach for bladder cancer, a replication-deficient adenovirus vector encoding a wild-type Rb, AdCMVRb, was constructed and transfected into the cultured human bladder carcinoma cell line EJ. The efficiency of gene transfection and expression was detected by immunochemical staining, Western blotting and polymerase chain reaction. The role of Rb in suppressing EJ growth was observed by cell-counting, [3H]thymidine incorporation and flow cytometry. The results showed that wild-type Rb gene could be transfected effectively into cultured EJ with Ad-CMVRb and could arrest the cells at GO/Gl phases of the cell cycle, leading to inhibition of DNA synthesis. The results demonstrated the potential of adenovirus-mediated Rb gene therapy for bladder cancer.
1998, 5(1):24-27.
DOI: 10.3872/j.issn.1007-385X.1998.1.008
Abstract:
将IL-2或/和IFN-γ基因体内转染腹腔巨噬细胞(MΦ),其表达的基因产物能提高MΦ的细胞毒活性,并诱导MΦ分泌TNF、IL-1和NO等抗肿瘤免疫介质.激发机体的非特异性免疫功能而产生抗肿瘤效应,特别是IL-2和IFN-γ基因联合转染MΦ,其表达的基因产物既能使MΦ产生更强的细胞毒活性并分泌高水平的TNF、IL-1和NO,又能激活脾CTL细胞,从而激发机体的非特异性和特异性免疫功能,产生更强的快同抗肿瘤效应.结果表明,IL-2和IFN-γ基因转染MΦ较单基因转染具有更强的抗瘤效应
将IL-2或/和IFN-γ基因体内转染腹腔巨噬细胞(MΦ),其表达的基因产物能提高MΦ的细胞毒活性,并诱导MΦ分泌TNF、IL-1和NO等抗肿瘤免疫介质.激发机体的非特异性免疫功能而产生抗肿瘤效应,特别是IL-2和IFN-γ基因联合转染MΦ,其表达的基因产物既能使MΦ产生更强的细胞毒活性并分泌高水平的TNF、IL-1和NO,又能激活脾CTL细胞,从而激发机体的非特异性和特异性免疫功能,产生更强的快同抗肿瘤效应.结果表明,IL-2和IFN-γ基因转染MΦ较单基因转染具有更强的抗瘤效应
1998, 5(1):28-31.
DOI: 10.3872/j.issn.1007-385X.1998.1.009
Abstract:
Escherichia coli cytosine deaminase ( CD) gene was transfected into murine B16F10 melanoma cells by recombinant adenovirus AdCD in vitro . The tumor cells infected with AdCD were more sensitive to 5-fluorocytosine (5FC) than cells infected with a control adenovirus AdLacZ. The supernatant from B16F10 cells treated with AdCD/5FC was transferred to uninfected cells, and we found that only 6. 25 % of the supernatant could significantly inhibit the growth of wild type B16F10 cells. When AdCD was directly injected into established subcutaneous B16F10 tumors in mice followed by intraperitoneal injection of 5FC for 10 days, a significant reduction in tumor size and prolongation of survival period were observed. These studies not only explored the cytotoxic effects of AdCD/5FC on B16F10 melanoma cells in vitro and in vivo but also elucidated the mechanisms of its bvstander effect.
Escherichia coli cytosine deaminase ( CD) gene was transfected into murine B16F10 melanoma cells by recombinant adenovirus AdCD in vitro . The tumor cells infected with AdCD were more sensitive to 5-fluorocytosine (5FC) than cells infected with a control adenovirus AdLacZ. The supernatant from B16F10 cells treated with AdCD/5FC was transferred to uninfected cells, and we found that only 6. 25 % of the supernatant could significantly inhibit the growth of wild type B16F10 cells. When AdCD was directly injected into established subcutaneous B16F10 tumors in mice followed by intraperitoneal injection of 5FC for 10 days, a significant reduction in tumor size and prolongation of survival period were observed. These studies not only explored the cytotoxic effects of AdCD/5FC on B16F10 melanoma cells in vitro and in vivo but also elucidated the mechanisms of its bvstander effect.
1998, 5(1):32-35.
DOI: 10.3872/j.issn.1007-385X.1998.1.010
Abstract:
本研究应用PHA、抗CD3单抗(aCD3)和rIL-2共同刺激人外周血单个核细胞(PBMC),诱生、扩增新型抗肿瘤效应细胞PHA-aCD3LAN,并与PHA-LAk和CD3AK细胞在某些生物学特性方面进行了比较,结果表明,PHA、aCD3和IL-2具有协同增强效应、使PHA-aCD3LAK细胞的增殖能力、细胞毒活性、mIL-2Ra的表达水平及对IL-2的利用均高于PHA-LAK和CD3AK细胞;三组效应细胞均为异质性细胞群体,均以CD3~+ CD8~+T细胞为主,而PHA-aCD3LAK的CD8~+细胞百分率高于其它两组细胞.采用PHA-aCD3LAK可进一步提高LAK细胞的数量和活性,具有重要的临床应用前景
本研究应用PHA、抗CD3单抗(aCD3)和rIL-2共同刺激人外周血单个核细胞(PBMC),诱生、扩增新型抗肿瘤效应细胞PHA-aCD3LAN,并与PHA-LAk和CD3AK细胞在某些生物学特性方面进行了比较,结果表明,PHA、aCD3和IL-2具有协同增强效应、使PHA-aCD3LAK细胞的增殖能力、细胞毒活性、mIL-2Ra的表达水平及对IL-2的利用均高于PHA-LAK和CD3AK细胞;三组效应细胞均为异质性细胞群体,均以CD3~+ CD8~+T细胞为主,而PHA-aCD3LAK的CD8~+细胞百分率高于其它两组细胞.采用PHA-aCD3LAK可进一步提高LAK细胞的数量和活性,具有重要的临床应用前景
Dai Shengming
,
Xiao Guiyuan
,
Zhou Shaoxiong
,
Rao Yingzhu
,
Zheng Xingwu
,
Zhou Ganping
,
Wu Maolian
1998, 5(1):36-38.
DOI: 10.3872/j.issn.1007-385X.1998.1.011
Abstract:
The effect of rhGM-CSF/IL-3 on apoptosis of Ara-C-induced myeloid leukemic cell line HL- 60 was investigated. The results indicated that treatment with rhGM-CSF/IL-3 in combination with Ara-C significantly inhibited the colony growth of HL-60 and enhanced the oligonucleosomal DNA fragmentation as compared with Ara-C alone. The Ara-C mediated apoptosis rates of HL-60 cells treated with rhGM-CSF/IL-3 fusion protein alone were markablely improved compared with treatment with rhIL-3 plus rhGM-CSF, it was noted that the Ara-C mediated of apoptosis normal peripheral white blood cells was less affected by rhGM-CSF/IL-3. It suggested that rhGM-CSF/IL-3 could be used as a possible curing drug during the phase of induced remission of leukemia.
The effect of rhGM-CSF/IL-3 on apoptosis of Ara-C-induced myeloid leukemic cell line HL- 60 was investigated. The results indicated that treatment with rhGM-CSF/IL-3 in combination with Ara-C significantly inhibited the colony growth of HL-60 and enhanced the oligonucleosomal DNA fragmentation as compared with Ara-C alone. The Ara-C mediated apoptosis rates of HL-60 cells treated with rhGM-CSF/IL-3 fusion protein alone were markablely improved compared with treatment with rhIL-3 plus rhGM-CSF, it was noted that the Ara-C mediated of apoptosis normal peripheral white blood cells was less affected by rhGM-CSF/IL-3. It suggested that rhGM-CSF/IL-3 could be used as a possible curing drug during the phase of induced remission of leukemia.
1998, 5(1):39-42.
DOI: 10.3872/j.issn.1007-385X.1998.1.012
Abstract:
After murine fetal liver cells (FLC) were transfected with granulocyte-macrophage colony-stimulating factor (GM-CSF) gene by recombinant adenovirus and intrasplenically transplanted into allogeneic mice, the effects of GM-CSF gene-transfected FLC on the recovery of immune response inhibited by chemotherapy were observed. The number of CD4 cells and the ratio of CD4 /CDS cells from peripheral blood lymphocytes increased significantly. The cytotoxicity of the NK cells and the proliferation response of splenocytes to ConA, LPS elevated markedly, but the same results were not from bone marrow. These data demonstrated that intrasplenic transplantation of GM-CSF gene-transfected FLC could effectively accelerate the recovery of immune response after high-dose chemotherapy.
After murine fetal liver cells (FLC) were transfected with granulocyte-macrophage colony-stimulating factor (GM-CSF) gene by recombinant adenovirus and intrasplenically transplanted into allogeneic mice, the effects of GM-CSF gene-transfected FLC on the recovery of immune response inhibited by chemotherapy were observed. The number of CD4 cells and the ratio of CD4 /CDS cells from peripheral blood lymphocytes increased significantly. The cytotoxicity of the NK cells and the proliferation response of splenocytes to ConA, LPS elevated markedly, but the same results were not from bone marrow. These data demonstrated that intrasplenic transplantation of GM-CSF gene-transfected FLC could effectively accelerate the recovery of immune response after high-dose chemotherapy.
1998, 5(1):43-44.
DOI: 10.3872/j.issn.1007-385X.1998.1.013
Abstract:
p16 gene was a tumor supressor gene found recently. The p16 protein is a negative regulator of cell proliferation . Loss of normal p16 function is associated with the development of neoplasms. To detect antitumorigenic effect of p16 on human lung adenocarcinoma cells, we cloned a p16 cDNA into the pcDNA3 vector at the sites of BamHl and Xho I to gain a p16 gene recombinant expression vector plasmid. We then transferred the p16 gene recombinant plasmid into human lung adenocarcinoma cell line (NCI-H460) by electroporation method. After G418 selection we assessed cell growth properties and cell cycle pattern by flow cytometry to G418-resistant clones of NCI-H460-pl6 and NCI-H460-vect respectively. The results show that human p16 gene could suppress the phenotype of NCI-H460 cell line and p16 gene therapy plays a positive role in human lung adenocarcinoma treatment.
p16 gene was a tumor supressor gene found recently. The p16 protein is a negative regulator of cell proliferation . Loss of normal p16 function is associated with the development of neoplasms. To detect antitumorigenic effect of p16 on human lung adenocarcinoma cells, we cloned a p16 cDNA into the pcDNA3 vector at the sites of BamHl and Xho I to gain a p16 gene recombinant expression vector plasmid. We then transferred the p16 gene recombinant plasmid into human lung adenocarcinoma cell line (NCI-H460) by electroporation method. After G418 selection we assessed cell growth properties and cell cycle pattern by flow cytometry to G418-resistant clones of NCI-H460-pl6 and NCI-H460-vect respectively. The results show that human p16 gene could suppress the phenotype of NCI-H460 cell line and p16 gene therapy plays a positive role in human lung adenocarcinoma treatment.
1998, 5(1):44-45.
DOI: 10.3872/j.issn.1007-385X.1998.1.014
Abstract:
Interleukin-17 (IL-17) is a newly found cytokine secreted by activated T lymphocytes. From preliminary study, IL-17 was found to play a role in the relationship between T lymphocytes and hematopoiesis, but many of its characteristics remain unknown up to now. To investigate its biological functions and related mechanisms, we cloned the complete coding region of human IL-17(hIL-17) from activated human peripheral blood mononuclear cells (PBMC) by RT-PCR and constructed an integrative vector pLCM182-hIL-17 for cloning, expressing and sequencing the hIL-17 gene. By DNA sequencing, the cloned hIL-17 is identical to the reptorted, and with temperature inducing, the hEL-17 was highly expressed in E. coli up to 30% of bacterial protein. The expressed hIL-17 protein could stimulate primary human fibrob-lasts to secrete IL-6 and GM-CSF after initial purification. This results indicate that the expressed hIL-17 has biological activity.
Interleukin-17 (IL-17) is a newly found cytokine secreted by activated T lymphocytes. From preliminary study, IL-17 was found to play a role in the relationship between T lymphocytes and hematopoiesis, but many of its characteristics remain unknown up to now. To investigate its biological functions and related mechanisms, we cloned the complete coding region of human IL-17(hIL-17) from activated human peripheral blood mononuclear cells (PBMC) by RT-PCR and constructed an integrative vector pLCM182-hIL-17 for cloning, expressing and sequencing the hIL-17 gene. By DNA sequencing, the cloned hIL-17 is identical to the reptorted, and with temperature inducing, the hEL-17 was highly expressed in E. coli up to 30% of bacterial protein. The expressed hIL-17 protein could stimulate primary human fibrob-lasts to secrete IL-6 and GM-CSF after initial purification. This results indicate that the expressed hIL-17 has biological activity.
1998, 5(1):48-49.
DOI: 10.3872/j.issn.1007-385X.1998.1.016
Abstract:
In order to study the bladder carcinoma cell growth suppression by introduction of foreign retinoblastoma (Rb) gene and explore a gene therapy approach for bladder cancer, a replication-deficient adenovirus vector encoding a wild-type Rb, AdCMVRb, was constructed and transfected into the cultured human bladder carcinoma cell line EJ. The efficiency of gene transfection and expression was detected by immunochemical staining, Western blotting and polymerase chain reaction. The role of Rb in suppressing EJ growth was observed by cell-counting, [3H]thymidine incorporation and flow cytometry. The results showed that wild-type Rb gene could be transfected effectively into cultured EJ with Ad-CMVRb and could arrest the cells at GO/Gl phases of the cell cycle, leading to inhibition of DNA synthesis. The results demonstrated the potential of adenovirus-mediated Rb gene therapy for bladder cancer.
In order to study the bladder carcinoma cell growth suppression by introduction of foreign retinoblastoma (Rb) gene and explore a gene therapy approach for bladder cancer, a replication-deficient adenovirus vector encoding a wild-type Rb, AdCMVRb, was constructed and transfected into the cultured human bladder carcinoma cell line EJ. The efficiency of gene transfection and expression was detected by immunochemical staining, Western blotting and polymerase chain reaction. The role of Rb in suppressing EJ growth was observed by cell-counting, [3H]thymidine incorporation and flow cytometry. The results showed that wild-type Rb gene could be transfected effectively into cultured EJ with Ad-CMVRb and could arrest the cells at GO/Gl phases of the cell cycle, leading to inhibition of DNA synthesis. The results demonstrated the potential of adenovirus-mediated Rb gene therapy for bladder cancer.
1998, 5(1):52-52.
DOI: 10.3872/j.issn.1007-385X.1998.1.019
Abstract:
本研究应用PHA、抗CD3单抗(aCD3)和rIL-2共同刺激人外周血单个核细胞(PBMC),诱生、扩增新型抗肿瘤效应细胞PHA-aCD3LAN,并与PHA-LAk和CD3AK细胞在某些生物学特性方面进行了比较,结果表明,PHA、aCD3和IL-2具有协同增强效应、使PHA-aCD3LAK细胞的增殖能力、细胞毒活性、mIL-2Ra的表达水平及对IL-2的利用均高于PHA-LAK和CD3AK细胞;三组效应细胞均为异质性细胞群体,均以CD3~ CD8~ T细胞为主,而PHA-aCD3LAK的CD8~ 细胞百分率高于其它两组细胞.采用PHA-aCD3LAK可进一步提高LAK细胞的数量和活性,具有重要的临床应用前景
本研究应用PHA、抗CD3单抗(aCD3)和rIL-2共同刺激人外周血单个核细胞(PBMC),诱生、扩增新型抗肿瘤效应细胞PHA-aCD3LAN,并与PHA-LAk和CD3AK细胞在某些生物学特性方面进行了比较,结果表明,PHA、aCD3和IL-2具有协同增强效应、使PHA-aCD3LAK细胞的增殖能力、细胞毒活性、mIL-2Ra的表达水平及对IL-2的利用均高于PHA-LAK和CD3AK细胞;三组效应细胞均为异质性细胞群体,均以CD3~ CD8~ T细胞为主,而PHA-aCD3LAK的CD8~ 细胞百分率高于其它两组细胞.采用PHA-aCD3LAK可进一步提高LAK细胞的数量和活性,具有重要的临床应用前景
1998, 5(1):53-53.
DOI: 10.3872/j.issn.1007-385X.1998.1.020
Abstract:
The effect of rhGM-CSF/IL-3 on apoptosis of Ara-C-induced myeloid leukemic cell line HL- 60 was investigated. The results indicated that treatment with rhGM-CSF/IL-3 in combination with Ara-C significantly inhibited the colony growth of HL-60 and enhanced the oligonucleosomal DNA fragmentation as compared with Ara-C alone. The Ara-C mediated apoptosis rates of HL-60 cells treated with rhGM-CSF/IL-3 fusion protein alone were markablely improved compared with treatment with rhIL-3 plus rhGM-CSF, it was noted that the Ara-C mediated of apoptosis normal peripheral white blood cells was less affected by rhGM-CSF/IL-3. It suggested that rhGM-CSF/IL-3 could be used as a possible curing drug during the phase of induced remission of leukemia.
The effect of rhGM-CSF/IL-3 on apoptosis of Ara-C-induced myeloid leukemic cell line HL- 60 was investigated. The results indicated that treatment with rhGM-CSF/IL-3 in combination with Ara-C significantly inhibited the colony growth of HL-60 and enhanced the oligonucleosomal DNA fragmentation as compared with Ara-C alone. The Ara-C mediated apoptosis rates of HL-60 cells treated with rhGM-CSF/IL-3 fusion protein alone were markablely improved compared with treatment with rhIL-3 plus rhGM-CSF, it was noted that the Ara-C mediated of apoptosis normal peripheral white blood cells was less affected by rhGM-CSF/IL-3. It suggested that rhGM-CSF/IL-3 could be used as a possible curing drug during the phase of induced remission of leukemia.
1998, 5(1):54-57.
DOI: 10.3872/j.issn.1007-385X.1998.1.021
Abstract:
After murine fetal liver cells (FLC) were transfected with granulocyte-macrophage colony-stimulating factor (GM-CSF) gene by recombinant adenovirus and intrasplenically transplanted into allogeneic mice, the effects of GM-CSF gene-transfected FLC on the recovery of immune response inhibited by chemotherapy were observed. The number of CD4 cells and the ratio of CD4 /CDS cells from peripheral blood lymphocytes increased significantly. The cytotoxicity of the NK cells and the proliferation response of splenocytes to ConA, LPS elevated markedly, but the same results were not from bone marrow. These data demonstrated that intrasplenic transplantation of GM-CSF gene-transfected FLC could effectively accelerate the recovery of immune response after high-dose chemotherapy.
After murine fetal liver cells (FLC) were transfected with granulocyte-macrophage colony-stimulating factor (GM-CSF) gene by recombinant adenovirus and intrasplenically transplanted into allogeneic mice, the effects of GM-CSF gene-transfected FLC on the recovery of immune response inhibited by chemotherapy were observed. The number of CD4 cells and the ratio of CD4 /CDS cells from peripheral blood lymphocytes increased significantly. The cytotoxicity of the NK cells and the proliferation response of splenocytes to ConA, LPS elevated markedly, but the same results were not from bone marrow. These data demonstrated that intrasplenic transplantation of GM-CSF gene-transfected FLC could effectively accelerate the recovery of immune response after high-dose chemotherapy.
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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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Chinese Journal Of Cancer Biotheray ® 2025 All Rights Reserved
Supported by:Beijing E-Tiller Technology Development Co., Ltd.