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| 1 | Cationic liposome-mediated transfection of CD40 ligand gene inhibits hepatic tumor growth of hepatocellular carcinoma in mice显示文摘Objective: To evaluate the efficacy of cationic liposome-mediated CD40 ligand (CD40L) gene therapy for hepato- cellular carcinoma. Methods: 1×106 of parental H22 cells or H22 cells transfected with the expression vector containing murine CD40L cDNA encoding the entire coding region (pcDNA3.1+-mCD40L) were inoculated subcutaneously into the left flanks of syngenic BALB/C mice. The tumor-bearing mice (tumor nodules 10 mm in maximal diameter) received the treatment of the intratumoral injection of pcDNA3.1+-mCD40L/Transfectam, pcDNA3.1+, or phosphate-buffered saline (PBS), or no treatment. The mice were monitored for tumor growth weekly. We examined mCD40L messenger ribonucleic acid (mRNA) expression by reverse transcription polymerase chain reaction (RT-PCR) and the histologic changes in tumors at two weeks after intratumoral injection using immunohistochemical staining of tumor tissues. Results: All mice inoculated with parental H22 cells developed a tumor subcutaneously, and the tumor size increased progressively within three weeks. However, the mice receiving H22-CD40L cells exhibited complete regression of the tumor two weeks after tumor cell inoculation. The tumor-bearing animals with the treatment of pcDNA3.1+ or PBS, or without treatment had progressive tumor growth, while those mice treated with pcDNA3.1+-mCD40L exhibited a significant inhibition of tumor growth. RT-PCR analysis showed that 783-bp fragments cor- responding to the mCD40L mRNA were amplified only from pcDNA3.1+-mCD40L treated tumors. The tumor samples from pcDNA3.1+-mCD40L-treated mice showed significant lymphocyte infiltration, apoptotic bodies, and confluent necrosis in the tumor tissues. Conclusion: The tumorigenicity of CD40L-expressing cells was abrogated when the cells were implanted subcu- taneously. In vivo gene therapy of established liver tumor nodules in mice by the intratumoral injection of pcDNA3.1+-mCD40L led to significant tumor inhibition. There was mCD40L mRNA expression in the tissues from pcDNA3.1+-mCD40L-treated tumors. The intratumoral injection of pcDNA3.1+-mCD40L induced a strong inflammatory, mainly lymphocytic infiltration of the tumor, and increased the necrotic rate of the neoplastic cells. | Yong-fang JIANG Jing MA Yan HE Yong-hong ZHANG Yun XU Guo-zhong GONG | 2009 | Journal of Zhejiang University-Science B(Biomedicine & Biotechnology)2009，10，1： | 3 |
| 2 | CD40配体基因对实验性肝细胞癌的治疗作用显示文摘目的:探讨鼠CD40配体基因体内抗肿瘤作用方法:转染和未转染质粒pcDNA3.1+-mCD40L的H22细胞(1×106)分别种植到同源Balb/c小鼠左侧腹皮下.荷瘤小鼠(瘤结节最大直径约10mm)瘤结节内直接注射pcDNA3.1+-mCD40L/脂质体复合物(治疗组)或者pcDNA3.1+、脂质体、培养基(对照组).每周测量各组小鼠皮下肿瘤结节的平均直径的大小,绘制肿瘤生长曲线.RT-PCR法检测治疗组肿瘤组织mCD40LmRNA的表达.常规组织HE染色观察治疗组肿瘤组织病理变化.结果:注射转染了质粒的H22细胞的Balb/c小鼠皮下一直未见瘤结节出现.治疗组荷瘤小鼠瘤结节生长受到明显的抑制,而对照组小鼠瘤结节生长没有抑制.用RT—PCR法从pcDNA3.1+-mCD40L治疗组的小鼠肿瘤组织中扩增出783bp大小片段产物.病理检查发现治疗组肿瘤组织中有明显淋巴细胞浸润、大量凋亡小体和片状坏死.结论:质粒pcDNA3.1+-mCD40L转染后使H22细胞致瘤性明显下降.直接瘤内注射pcDNA3.1+-mCD40L能使荷瘤Balb/c小鼠瘤结节生长明显抑制.质粒pcDNA3.1+-mCD40L治疗组肿瘤组织中有mCD40LmRNA的表达和明显的炎症反应以及肿瘤细胞凋亡、坏死明显增加. | 蒋永芳 何艳 张永红 许允 龚国忠 | 2005 | 世界华人消化杂志2005，13，11： | 0 |
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