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Volume 13,Issue 1,2006 Table of Contents
2006, 13(1):1-2.
DOI: 10.3872/j.issn.1007-385X.2006.1.001
Abstract:
肿瘤的抗体治疗指用特异性抗体或抗体片段治疗肿瘤, 是当前医药学研究的热点之一。造血系统肿瘤包括淋巴瘤和白血病,虽然放疗和化疗可缓解大多数造血系统肿瘤,但仍存在复发和治疗无效(难治)的患者。抗体治疗以其较高的有效率和安全性为复发和难治的患者提供了一种选择。
肿瘤的抗体治疗指用特异性抗体或抗体片段治疗肿瘤, 是当前医药学研究的热点之一。造血系统肿瘤包括淋巴瘤和白血病,虽然放疗和化疗可缓解大多数造血系统肿瘤,但仍存在复发和治疗无效(难治)的患者。抗体治疗以其较高的有效率和安全性为复发和难治的患者提供了一种选择。
ZHANG Guo-yun
,
LIU Na
,
ZHANG Si-yuan
,
PAN Yang-lin
,
SUN Li-jun
,
HONG Liu
,
HAO Zhi-ming
,
QIAO Tai-dong
,
CHEN Zheng
,
FAN Dai-ming
,
BI Feng
2006, 13(1):3-7.
DOI: 10.3872/j.issn.1007-385X.2006.1.002
Abstract:
To study the effect of RhoC on the metastasis of gastric cancer cells. Methods: A group of RhoC -specific small interfering RNAs (siHNA) were designed and the related vectors were constructed with the assistance of computer. The vectors were transfected into human gastric cancer cell SGC7901 by Iipofectamine2000. The protein expression of RhoC in the translectants was examined by Western blot.Cell growth rate was determined will a Cell Counting Kit -8. MTT assay was used to evaluate the sensitivity of the transfectants to anticancer drugs. Wound-healing and invasion assays were used to examine the abilities of migration and invasion, respectively. Results:Five RhoC-specif-ic siRNAs were designed and the related vectors were constructed successfully. Western blot showed that RhoC-specific siRNA, RhoC-s362, dramatically inhibited RhoC expression. Though down-regulation of RhoC expression did not affect the proliferation and chemo-sensitivity of the transfectants; it did suppress the migrating and invasive abilities of gastric cancer cells. Conclusion: RhoC siRNA RhoC-s362 can effectively inhibit RhoC expression and restrain the migration and invasion of the SGC7901 , suggesting that RhoC play an important role in the metastasis of gastric cancer.
To study the effect of RhoC on the metastasis of gastric cancer cells. Methods: A group of RhoC -specific small interfering RNAs (siHNA) were designed and the related vectors were constructed with the assistance of computer. The vectors were transfected into human gastric cancer cell SGC7901 by Iipofectamine2000. The protein expression of RhoC in the translectants was examined by Western blot.Cell growth rate was determined will a Cell Counting Kit -8. MTT assay was used to evaluate the sensitivity of the transfectants to anticancer drugs. Wound-healing and invasion assays were used to examine the abilities of migration and invasion, respectively. Results:Five RhoC-specif-ic siRNAs were designed and the related vectors were constructed successfully. Western blot showed that RhoC-specific siRNA, RhoC-s362, dramatically inhibited RhoC expression. Though down-regulation of RhoC expression did not affect the proliferation and chemo-sensitivity of the transfectants; it did suppress the migrating and invasive abilities of gastric cancer cells. Conclusion: RhoC siRNA RhoC-s362 can effectively inhibit RhoC expression and restrain the migration and invasion of the SGC7901 , suggesting that RhoC play an important role in the metastasis of gastric cancer.
WANG Xiao-bing
,
LI Mo
,
LIU Zhao-yang
,
TIAN Hai-mei
,
QU Ping
,
LI Yan-fen
,
LIU Yi
,
CAO Dong-yan
,
LIANG Zhi
,
CHENG Dong -wan
,
SHAO Chang-jun
,
ZHANG Wei
2006, 13(1):8-12.
DOI: 10.3872/j.issn.1007-385X.2006.1.003
Abstract:
To study the biological effects of the HPV16Z-Hsp65-E6/E7 fusion protein vaccine on the tumor associated with HPV16 infection. Methods: We tested the cellular immune responsive intensity to the vaccine by the lymphocyte proliferation and CTL response, and studied the therapeutic effect of the vaccine on mouse TC-1 cell transplanted cancer in vivo and the influence on mouse lifetime. Results: The spleen lymphocytes from the C57BL/6 mouse immunized by the Hsp65-E6/E7 vaccine could proliferate obviously in the presence of the protein and TC-1 tumor cell could be lysed specifically by immune activated lymphocytes in vitro. This animal therapeutic experiment in vivo showed that the vaccine suppressed the growth of TC-1 cell transplanted tumor remarkably. Conclusion: The recombined vaccine can induce specific cellular immune response in vitro and suppress HPV16 positive TC-1 tumor cell growth obviously in vivo.
To study the biological effects of the HPV16Z-Hsp65-E6/E7 fusion protein vaccine on the tumor associated with HPV16 infection. Methods: We tested the cellular immune responsive intensity to the vaccine by the lymphocyte proliferation and CTL response, and studied the therapeutic effect of the vaccine on mouse TC-1 cell transplanted cancer in vivo and the influence on mouse lifetime. Results: The spleen lymphocytes from the C57BL/6 mouse immunized by the Hsp65-E6/E7 vaccine could proliferate obviously in the presence of the protein and TC-1 tumor cell could be lysed specifically by immune activated lymphocytes in vitro. This animal therapeutic experiment in vivo showed that the vaccine suppressed the growth of TC-1 cell transplanted tumor remarkably. Conclusion: The recombined vaccine can induce specific cellular immune response in vitro and suppress HPV16 positive TC-1 tumor cell growth obviously in vivo.
2006, 13(1):13-17.
DOI: 10.3872/j.issn.1007-385X.2006.1.004
Abstract:
观察重组人软骨调节素（chondromodulin，CHM）蛋白对骨肿瘤的治疗作用。方法：利用RT-PCR技术从人软骨组织中扩增出CHM—I基因片段，并将其克隆到原核表达载体pET28a，在大肠杆菌中诱导表达和纯化重组人软骨调节素蛋白，将重组蛋白与人脐静脉上皮细胞或MG-63骨肉瘤细胞共培养，观察其对内皮细胞形成管样结构和MG-63骨肉瘤细胞生长的影响；将重组蛋白局部注射裸鼠皮下肿瘤，观察其对肿瘤形成的影响。结果：获得纯化的重组人软骨调节素蛋白，该蛋白在体外可以抑制血管内皮细胞管样结构的形成而对肿瘤细胞的生长无影响；重组蛋白瘤内注射可以抑制肿瘤在裸鼠体内的生长。结论：重组人软骨调节索蛋白通过抑制血管形成而抑制肿瘤生长，具有良好的临床应用价值。
观察重组人软骨调节素（chondromodulin，CHM）蛋白对骨肿瘤的治疗作用。方法：利用RT-PCR技术从人软骨组织中扩增出CHM—I基因片段，并将其克隆到原核表达载体pET28a，在大肠杆菌中诱导表达和纯化重组人软骨调节素蛋白，将重组蛋白与人脐静脉上皮细胞或MG-63骨肉瘤细胞共培养，观察其对内皮细胞形成管样结构和MG-63骨肉瘤细胞生长的影响；将重组蛋白局部注射裸鼠皮下肿瘤，观察其对肿瘤形成的影响。结果：获得纯化的重组人软骨调节素蛋白，该蛋白在体外可以抑制血管内皮细胞管样结构的形成而对肿瘤细胞的生长无影响；重组蛋白瘤内注射可以抑制肿瘤在裸鼠体内的生长。结论：重组人软骨调节索蛋白通过抑制血管形成而抑制肿瘤生长，具有良好的临床应用价值。
2006, 13(1):22-26.
DOI: 10.3872/j.issn.1007-385X.2006.1.006
Abstract:
investigate whether phosphorothioate-modified antisense vascular endothelial growth factor oligodeoxynucleotides ( VEGF-ASODN) formulated in cationic liposome can inhibit the blood flow of lung cancer. Methods: Lewis lung tumor models were established by subcutaneous injection of Lewis lung carcinoma cells into the right flank of 40 C57BL/6 mice. Twenty-four hours later, mice were randomly assigned into 4 groups; pure liposome, liposome containing ASODN, SODN and MODN. Mice in each group were treated twice a week for 4 weeks. Tumor growth were determined. Peak systolic flow velocity (PS) and resistance index (RI) were measured with a sonographic scanner. Expression of VEGF mRNA were detected by hybridization in situ and RT-PCR. Results: ASODN significantly suppressed the growth of subcutaneous tumors. PS and RI in VEGF-ASODN group were significantly different from those in other 3 groups ( P < 0. 01 ). ASODN markedly downregulated the expression of VEGF at level of mRNA. Conclusion:It is demonstrated that the phosphorothioate-modified ASODN can significantly suppress the growth of tumor by damaging the blood flow of lung cancer.
investigate whether phosphorothioate-modified antisense vascular endothelial growth factor oligodeoxynucleotides ( VEGF-ASODN) formulated in cationic liposome can inhibit the blood flow of lung cancer. Methods: Lewis lung tumor models were established by subcutaneous injection of Lewis lung carcinoma cells into the right flank of 40 C57BL/6 mice. Twenty-four hours later, mice were randomly assigned into 4 groups; pure liposome, liposome containing ASODN, SODN and MODN. Mice in each group were treated twice a week for 4 weeks. Tumor growth were determined. Peak systolic flow velocity (PS) and resistance index (RI) were measured with a sonographic scanner. Expression of VEGF mRNA were detected by hybridization in situ and RT-PCR. Results: ASODN significantly suppressed the growth of subcutaneous tumors. PS and RI in VEGF-ASODN group were significantly different from those in other 3 groups ( P < 0. 01 ). ASODN markedly downregulated the expression of VEGF at level of mRNA. Conclusion:It is demonstrated that the phosphorothioate-modified ASODN can significantly suppress the growth of tumor by damaging the blood flow of lung cancer.
2006, 13(1):27-31.
DOI: 10.3872/j.issn.1007-385X.2006.1.007
Abstract:
To investigate the proliferation and apoptosis of human osteosarcoma cell line U-2OS after sur-vivin gene was knocked down by siRNA synthesized in vitro. Methods: U-2OS cells were divided into 3 groups: Group A (blank control) , group B ( transfected with non-specific siRNA) and group C( transfected with survivin-specific siRNA). The morphological changes of U-2OS cells were observed with fluorescent microscope. The expression of survivin mRNA and protein were detected by reverse transcription polymerase chain reaction ( RT-PCR) and Western blotting. The anti-proliferative effects were assessed by MTT and the rate of apoptosis was examined by flow cytometry in 3 groups. The results of the 3 groups were analyzed and compared. Results: Survivin specific siRNA significantly down-regulated mRNA and protein expression of survivin. Expression of survivin protein in group C was significantly lower than those in group A and B( P <0. 01 ) ; Group C also showed a slower proliferation than the other 2 groups ( P <0. 01 ). The apoptosis rate in group C was significantly higher than those in other 2 groups ( P <0.01 ). Conclusion: siRNA can efficiently suppress survivin gene expression, inhibit proliferation and induce apoptosis in osteosarcoma cell line U-2OS.
To investigate the proliferation and apoptosis of human osteosarcoma cell line U-2OS after sur-vivin gene was knocked down by siRNA synthesized in vitro. Methods: U-2OS cells were divided into 3 groups: Group A (blank control) , group B ( transfected with non-specific siRNA) and group C( transfected with survivin-specific siRNA). The morphological changes of U-2OS cells were observed with fluorescent microscope. The expression of survivin mRNA and protein were detected by reverse transcription polymerase chain reaction ( RT-PCR) and Western blotting. The anti-proliferative effects were assessed by MTT and the rate of apoptosis was examined by flow cytometry in 3 groups. The results of the 3 groups were analyzed and compared. Results: Survivin specific siRNA significantly down-regulated mRNA and protein expression of survivin. Expression of survivin protein in group C was significantly lower than those in group A and B( P <0. 01 ) ; Group C also showed a slower proliferation than the other 2 groups ( P <0. 01 ). The apoptosis rate in group C was significantly higher than those in other 2 groups ( P <0.01 ). Conclusion: siRNA can efficiently suppress survivin gene expression, inhibit proliferation and induce apoptosis in osteosarcoma cell line U-2OS.
2006, 13(1):37-41.
DOI: 10.3872/j.issn.1007-385X.2006.1.009
Abstract:
To observe the effects of RNAi-mediated survivin gene on silencing prostate cancer cell lines PC3. Methods: Three target gene fragments were cloned into pSilencerTM3. 1-H1 neo vector separately. Three recombinant eukaryotic expression vectors, pSilencer 3. 1-SVV1, pSilencer 3.1-SVV2 and pSilencer 3. 1-SVV3 were successfully constructed, then the recombinant vectors were transfected into prostate cancer cells PC3. After PC3 cells were transfected with recombinant vectors, the interference effects were detected by RT-PCR and Western blot. The apoptosis index and cell cycle of PC3 cells were detected by Flow cytometry. The survival curve of PC3 cells treated with Platinol and the proliferation of PC3 cells were detected by MTT. Results: The results of RT-PCR and Western blot indicated that pSilencer 3. 1-SVV2 and pSilencer 3. 1-SVV3 vectors could knock down the transcription and expression of survivin gene. After PC3 cells were transfected with pSilencer 3. 1-SVV2 and pSilencer 3. 1-SVV3 vectors, the apoptosis index of PC3 cells increased by about 10% -15% , the proliferation of PC3 cells become slowly and the cells number decreased about 30% compared with control groups. The cell number during G1 phases increased 10% and during G2 and S phases the cells number decreased about 5 % . After PC3 cells treated with Platinol, the survival rate of PC3 cells transfected with pSilencer 3.1-SW2 and pSilencer 3. 1-SVV3 vectors decreased by about 35% -45% and apoptosis index increased by about 10% -14% contrast with control groups. Conclusion: The study provides basis for study the function of survivin gene, indicating the survivin may be a new target of gene therapy on prostate cancer.
To observe the effects of RNAi-mediated survivin gene on silencing prostate cancer cell lines PC3. Methods: Three target gene fragments were cloned into pSilencerTM3. 1-H1 neo vector separately. Three recombinant eukaryotic expression vectors, pSilencer 3. 1-SVV1, pSilencer 3.1-SVV2 and pSilencer 3. 1-SVV3 were successfully constructed, then the recombinant vectors were transfected into prostate cancer cells PC3. After PC3 cells were transfected with recombinant vectors, the interference effects were detected by RT-PCR and Western blot. The apoptosis index and cell cycle of PC3 cells were detected by Flow cytometry. The survival curve of PC3 cells treated with Platinol and the proliferation of PC3 cells were detected by MTT. Results: The results of RT-PCR and Western blot indicated that pSilencer 3. 1-SVV2 and pSilencer 3. 1-SVV3 vectors could knock down the transcription and expression of survivin gene. After PC3 cells were transfected with pSilencer 3. 1-SVV2 and pSilencer 3. 1-SVV3 vectors, the apoptosis index of PC3 cells increased by about 10% -15% , the proliferation of PC3 cells become slowly and the cells number decreased about 30% compared with control groups. The cell number during G1 phases increased 10% and during G2 and S phases the cells number decreased about 5 % . After PC3 cells treated with Platinol, the survival rate of PC3 cells transfected with pSilencer 3.1-SW2 and pSilencer 3. 1-SVV3 vectors decreased by about 35% -45% and apoptosis index increased by about 10% -14% contrast with control groups. Conclusion: The study provides basis for study the function of survivin gene, indicating the survivin may be a new target of gene therapy on prostate cancer.
2006, 13(1):42-44.
DOI: 10.3872/j.issn.1007-385X.2006.1.010
Abstract:
To study the inhibitory effect of a double-strand small interfering RNA targeting Bcl-XL (Bcl-XL siRNA) in human colon cancer cells. Methods: Human colon cancer cell line DLD1 was treated with Bcl-XL siRNA, The protein level of Bcl-XL in the cells was determined by Western blot; the apoptotic ratio and survival condition were detected by flow cytometry assay and trypan blue-stained cell counting with hemocytometer, respectively. Results: The level of Bcl-XL protein in DLD1 cells was obviously down-regulated by Bcl-XL siRNA. The apoptotic ratio was significantly higher in Bcl-XL siRNA treated group than those in control (P<0.05) , whereas the survival rate of cells was significantly decreased in Bcl-XL siRNA group(P <0. 05). Conclusion: Bcl-XL siRNA can effectively knock down the Bcl-XL protein and inhibit the growth of human colon cancer cells, which might be a new way for colon cancer treatment.
To study the inhibitory effect of a double-strand small interfering RNA targeting Bcl-XL (Bcl-XL siRNA) in human colon cancer cells. Methods: Human colon cancer cell line DLD1 was treated with Bcl-XL siRNA, The protein level of Bcl-XL in the cells was determined by Western blot; the apoptotic ratio and survival condition were detected by flow cytometry assay and trypan blue-stained cell counting with hemocytometer, respectively. Results: The level of Bcl-XL protein in DLD1 cells was obviously down-regulated by Bcl-XL siRNA. The apoptotic ratio was significantly higher in Bcl-XL siRNA treated group than those in control (P<0.05) , whereas the survival rate of cells was significantly decreased in Bcl-XL siRNA group(P <0. 05). Conclusion: Bcl-XL siRNA can effectively knock down the Bcl-XL protein and inhibit the growth of human colon cancer cells, which might be a new way for colon cancer treatment.
2006, 13(1):50-53.
DOI: 10.3872/j.issn.1007-385X.2006.1.012
Abstract:
To establish abdomino-metastasis model of human ovarian carcinoma cell strain SKOV3 (over-expressed HER-2/neu) in nude mice, and to explore the inhibitory effect and mechanism of herceptin combined with cD-D? on mice model. Methods: Ninety-six hours after SKOV3 cell were implanted into abdominal cavity, nude mice were randomly divided into 4 groups: A group normal saline, B group cDDP, C group herceptin and D group herceptin plus cD-DP. The tumor formation rate, survival time and prolongation survival time of tumor-bearing nude mice were evaluated. The changes of Fas and FasL were estimated by flow cytometry( FCM). HER-2/neu in tissue of group A and D was detected with pathological and immunohistochemistry method. Results: HER-2/neu was overexpressed in abdominal cavity implanted with SKOV3 tumors; herceptin combined with cDDP decreased the contents of HER-2/neu. Herceptin and cDDP significantly inhibited abdomino-plantation of SKOV3 in nude mice, and prolonged their survival time. Flow cytometry showed significant difference in apoptosis rate between control group and other groups( P=0. 001 ). The highest apoptosis rate was 55. 9% in the combination group; the expression of FasL was not significantly different between control group and other groups. Conclusion: Herceptin and cDDP can inhibit the growth of SKOV3 cells and prolong the survival duration of tumor-bearing nude mice and the mechanism may be associated with the positive regulation of CD95.
To establish abdomino-metastasis model of human ovarian carcinoma cell strain SKOV3 (over-expressed HER-2/neu) in nude mice, and to explore the inhibitory effect and mechanism of herceptin combined with cD-D? on mice model. Methods: Ninety-six hours after SKOV3 cell were implanted into abdominal cavity, nude mice were randomly divided into 4 groups: A group normal saline, B group cDDP, C group herceptin and D group herceptin plus cD-DP. The tumor formation rate, survival time and prolongation survival time of tumor-bearing nude mice were evaluated. The changes of Fas and FasL were estimated by flow cytometry( FCM). HER-2/neu in tissue of group A and D was detected with pathological and immunohistochemistry method. Results: HER-2/neu was overexpressed in abdominal cavity implanted with SKOV3 tumors; herceptin combined with cDDP decreased the contents of HER-2/neu. Herceptin and cDDP significantly inhibited abdomino-plantation of SKOV3 in nude mice, and prolonged their survival time. Flow cytometry showed significant difference in apoptosis rate between control group and other groups( P=0. 001 ). The highest apoptosis rate was 55. 9% in the combination group; the expression of FasL was not significantly different between control group and other groups. Conclusion: Herceptin and cDDP can inhibit the growth of SKOV3 cells and prolong the survival duration of tumor-bearing nude mice and the mechanism may be associated with the positive regulation of CD95.
2006, 13(1):54-58.
DOI: 10.3872/j.issn.1007-385X.2006.1.013
Abstract:
To establish a mouse lymphopenia model via irradiation and to study its immune characteristics. Methods: Lymphocytes isolated from PBMC, spleen and inguinal lymph-nodes were counted after C57BL/6 mice were treated with irradiation at the dosage of 1. 25 Gy. Subsets of lymphocytes were analyzed by FACS. The expression of transcription factors T-bet and GATA-3 were detected by RT-PCR. Irradiated mice treated with DC-gp100 vaccine were challenged by B16F10 tumor cells, tumor growth was observed. Results: 1.25 Gy irradiation significantly decreased the cell number of lymphocytes, specially the subset of CD4+CD25 +T cells. A memory-like T subset was induced during the course of immune reconstitution. The expression of T-bet but not GATA-3 in the splenocytes was up-regulated. Irradiated mice vaccinated with DC-gplOO could resist the tumor challenge and retard the tumor growth. Conclusion: Lymphopenia mouse model is successfully established and an enhanced immune protection can be induced under the lymphopenia status.
To establish a mouse lymphopenia model via irradiation and to study its immune characteristics. Methods: Lymphocytes isolated from PBMC, spleen and inguinal lymph-nodes were counted after C57BL/6 mice were treated with irradiation at the dosage of 1. 25 Gy. Subsets of lymphocytes were analyzed by FACS. The expression of transcription factors T-bet and GATA-3 were detected by RT-PCR. Irradiated mice treated with DC-gp100 vaccine were challenged by B16F10 tumor cells, tumor growth was observed. Results: 1.25 Gy irradiation significantly decreased the cell number of lymphocytes, specially the subset of CD4+CD25 +T cells. A memory-like T subset was induced during the course of immune reconstitution. The expression of T-bet but not GATA-3 in the splenocytes was up-regulated. Irradiated mice vaccinated with DC-gplOO could resist the tumor challenge and retard the tumor growth. Conclusion: Lymphopenia mouse model is successfully established and an enhanced immune protection can be induced under the lymphopenia status.
2006, 13(1):59-62.
DOI: 10.3872/j.issn.1007-385X.2006.1.014
Abstract:
构建缺氧诱导的AFP基因启动子（HRE-AFPp）调控的基因表达载体，并检测该调控元件的特异性和对缺氧诱导的反应性。方法：用PCR方法从人类基因组中扩增VEGF基因缺氧反应元件（HRE）和AFP基因启动子（AFPp），将上述片段与含有报告基因（强化绿色荧光蛋白基因）载体pEGFP-1的多克隆位点连接，构建成为缺氧诱导的AFP基因启动予调控的基因表达载体（pEGFP-[HRE]AFPp）。用脂质体法将表达载体转染表达或不表达AFP的细胞系，G418筛选阳性克隆，荧光显微镜观测重组AFPp的活性，并用流式细胞术检测缺氧诱导是否对其有调控作用。结果：成功地将HRE、AFPp克隆到报告基因载体pEGFP-1的多克隆位点，酶切鉴定和DNA序列分析无误，荧光显微镜观测证实EGFP能在AFP阳性肝癌细胞特异性表达，流式细胞术检测证实，16h缺氧诱导能增强EGFP的表达（P〈0．01）。结论：缺氧诱导的AFP顺式作用元件修饰的基因治疗载体，在基因转录水平特异性调控目的基因的表达，为下一步将其作为肝癌基因治疗载体奠定了基础。
构建缺氧诱导的AFP基因启动子（HRE-AFPp）调控的基因表达载体，并检测该调控元件的特异性和对缺氧诱导的反应性。方法：用PCR方法从人类基因组中扩增VEGF基因缺氧反应元件（HRE）和AFP基因启动子（AFPp），将上述片段与含有报告基因（强化绿色荧光蛋白基因）载体pEGFP-1的多克隆位点连接，构建成为缺氧诱导的AFP基因启动予调控的基因表达载体（pEGFP-[HRE]AFPp）。用脂质体法将表达载体转染表达或不表达AFP的细胞系，G418筛选阳性克隆，荧光显微镜观测重组AFPp的活性，并用流式细胞术检测缺氧诱导是否对其有调控作用。结果：成功地将HRE、AFPp克隆到报告基因载体pEGFP-1的多克隆位点，酶切鉴定和DNA序列分析无误，荧光显微镜观测证实EGFP能在AFP阳性肝癌细胞特异性表达，流式细胞术检测证实，16h缺氧诱导能增强EGFP的表达（P〈0．01）。结论：缺氧诱导的AFP顺式作用元件修饰的基因治疗载体，在基因转录水平特异性调控目的基因的表达，为下一步将其作为肝癌基因治疗载体奠定了基础。
2006, 13(1):63-64.
DOI: 10.3872/j.issn.1007-385X.2006.1.015
Abstract:
表皮生长因子受体(epidermal growth factor recep- tor,EGFR)是一种具有酪氨酸激酶活性的跨膜表面受体,其介导的信号转导效应具有多向性,包括细胞增殖分化、迁移和内环境的稳定,并与细胞的再生和恶性转化密切相关,在人类多种恶性肿瘤中存在高表达。
表皮生长因子受体(epidermal growth factor recep- tor,EGFR)是一种具有酪氨酸激酶活性的跨膜表面受体,其介导的信号转导效应具有多向性,包括细胞增殖分化、迁移和内环境的稳定,并与细胞的再生和恶性转化密切相关,在人类多种恶性肿瘤中存在高表达。
2006, 13(1):65-66.
DOI: 10.3872/j.issn.1007-385X.2006.1.016
Abstract:
近年来研究表明胃癌的生长分化受多种胃肠肽类激素的凋控,生长抑素(somatostatin,SST)可能起重要的作用。本研究旨在探讨SST类似物奥曲肽(octreoti- de,OCT)对胃癌裸鼠种植瘤生长及侵袭转移的影响。 1材料与方法
近年来研究表明胃癌的生长分化受多种胃肠肽类激素的凋控,生长抑素(somatostatin,SST)可能起重要的作用。本研究旨在探讨SST类似物奥曲肽(octreoti- de,OCT)对胃癌裸鼠种植瘤生长及侵袭转移的影响。 1材料与方法
2006, 13(1):67-76.
DOI: 10.3872/j.issn.1007-385X.2006.1.017
Abstract:
诱骗受体3（decoy receptor3，DcR3）是肿瘤坏死因子受体超家族的新成员。它通过拮抗Fas／FasL系统及LIGHT／LTβR、LIGHT／HVEM／TR2系统的作用，在肿瘤及免疫性疾病中发挥重要作用。DcR3的基因位于20q13．3，在人肿瘤细胞中会发生基因扩增和重排；在多种肿瘤、自身免疫疾病中高表达；作用机制有LIGHT和配体FasL途径等；促肿瘤发生；可下凋宿主免疫功能，能降低T细胞对同种抗原应答，有重大开发潜能。
诱骗受体3（decoy receptor3，DcR3）是肿瘤坏死因子受体超家族的新成员。它通过拮抗Fas／FasL系统及LIGHT／LTβR、LIGHT／HVEM／TR2系统的作用，在肿瘤及免疫性疾病中发挥重要作用。DcR3的基因位于20q13．3，在人肿瘤细胞中会发生基因扩增和重排；在多种肿瘤、自身免疫疾病中高表达；作用机制有LIGHT和配体FasL途径等；促肿瘤发生；可下凋宿主免疫功能，能降低T细胞对同种抗原应答，有重大开发潜能。
2006, 13(1):70-76.
DOI: 10.3872/j.issn.1007-385X.2006.1.018
Abstract:
随着生物技术的发展,单抗靶向治疗肿瘤显示了良好前景。在基础研究领域,主要集中在将抗体与化学药物、酶、放射性核素、毒素和生物诱导剂等偶联后直接杀伤肿瘤或者利用抗体促进肿瘤细胞凋亡和抑制肿瘤血管生成等方面。在临床已有多种单抗药物投入使用,其中用于造血系统肿瘤的治疗效果较好,治疗实体肿瘤方面也取得了进展。
随着生物技术的发展,单抗靶向治疗肿瘤显示了良好前景。在基础研究领域,主要集中在将抗体与化学药物、酶、放射性核素、毒素和生物诱导剂等偶联后直接杀伤肿瘤或者利用抗体促进肿瘤细胞凋亡和抑制肿瘤血管生成等方面。在临床已有多种单抗药物投入使用,其中用于造血系统肿瘤的治疗效果较好,治疗实体肿瘤方面也取得了进展。
2006, 13(1):73-76.
DOI: 10.3872/j.issn.1007-385X.2006.1.019
Abstract:
4-1BB（CDl37）和4-1BB配体（4—1BBL）属于肿瘤坏死因子／肿瘤坏死因子受体（TNF／TNFR）超家族成员，在树突状细胞（DC）及部分T细胞上表达。4-1BB和4-1BBL相互作用，通过一系列信号转导，激发未成熟DC的分化成熟，并且通过TRAF2和MAPK途径，使未成熟Dc介导初始型T细胞活化进而向Thl型细胞转化，从而产生有效的记忆性CTL和效应性CTL。深人探讨4-1BB和4-1BBL的作用机制，可能为肿瘤等疾病的治疗提供新思路。
4-1BB（CDl37）和4-1BB配体（4—1BBL）属于肿瘤坏死因子／肿瘤坏死因子受体（TNF／TNFR）超家族成员，在树突状细胞（DC）及部分T细胞上表达。4-1BB和4-1BBL相互作用，通过一系列信号转导，激发未成熟DC的分化成熟，并且通过TRAF2和MAPK途径，使未成熟Dc介导初始型T细胞活化进而向Thl型细胞转化，从而产生有效的记忆性CTL和效应性CTL。深人探讨4-1BB和4-1BBL的作用机制，可能为肿瘤等疾病的治疗提供新思路。
联系方式
- 《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
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Chinese Journal Of Cancer Biotheray ® 2025 All Rights Reserved
Supported by:Beijing E-Tiller Technology Development Co., Ltd.