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TNFSF15表达下调或缺失对卵巢癌组织中肿瘤新血管形成的影响

The Effect of Down Regulation of TNFSF15 on Tumor Neovascularization of Ovarian Cancer
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摘要 目的:探讨肿瘤坏死因子超家族-15(TNFSF15)在人卵巢癌标本中的表达及在小鼠体内TNFSF15对卵巢癌血管生成及卵巢癌生长的影响。方法:应用免疫组化法检测正常组(12例)、卵巢癌组(94例)中TNFSF15的表达情况及微血管密度(MVD);雌性C57BL/6小鼠24只随机分为对照组、重组TNFSF15注射组(实验组)、TNFSF15-shRNA处理组(A组)、shRNA-对照组(B组),每组6只,各组均采用皮下注射ID8细胞制备小鼠荷瘤模型,实验组采用腹腔注射重组TNFSF15蛋白,A、B组采用TNFSF15-shRNA干扰其内源性表达的方法,通过检测小鼠肿瘤组织MVD值并测量肿瘤体积大小,观察其对小鼠卵巢癌细胞系ID8在小鼠C57BL/6体内血管生成及肿瘤生长的影响。结果:与正常卵巢组织相比,卵巢癌组织标本中TNFSF15表达显著降低(P<0.01),且Ⅲ/Ⅳ期TNFSF15阳性表达率较Ⅰ/Ⅱ期降低(P<0.05);实验组较对照组小鼠肿瘤组织中MVD值降低且肿瘤体积减小(P<0.05),而A组较B组MVD值升高且肿瘤体积增大(P<0.05)。结论:卵巢癌微环境中TNFSF15表达下调或缺失是肿瘤新血管形成的前提条件。 Objective: To study the expression of tumor necrosis factor superfamily-15 (TNFSF15) in human ovarian cancer specimens and the effects of TNFSF15 on tumor angiogenesis and growth in mice. Methods: The expression of TNFSFI5 and the value of microvesse] density (MVD) were detected by the method of immunohistochemistry in normal ovary group (n=12) and ovarian cancer group (n=94). Twenty-four female C57BId6 mice were randomly divided into 4 groups: control group, recombinant TNFSFI'5-treated group (experimental group), TNFSF15 shRNA-treated group (group A) and control-shRNA (group B). There were 6 mice for each group. The tumor-bearing mouse model was made by injecting subcutaneously ID8 cells into the flank of mia. The recombinant TNFSF15 was used to treat IDS-beafing C57BId6 mice via intraperitoneal injection. TNFSFI5-shRNA was used in group A and group B. The influences of TNFSF15 on tumor angiogenesis and growth were assessed by measuring MVD values and tumor volumes in mice. Results: Compared to the normal ovary tissues, the expression level of TNFSF15 decreased significantly in cancer specimens (P 〈 0.01), and the positive expression of TNFSF15 protein was lower in stage III/IV than that of stage I/II (P 〈 0.05). The values of MVD and the tumor volumes were decreased in experimental group than those of control group(P 〈 0.05). On the other hand, the MVD values and tumor volumes were higher in group A than those of group B(P 〈 0.05). Conclusion: The down regulation or absent of TNFSFI5 in ovarian cancer microenvironment is a pre-requisite for tumor neovaseularization.
出处 《天津医药》 CAS 北大核心 2012年第9期908-911,共4页 Tianjin Medical Journal
基金 国家自然科学基金资助项目(项目编号:30670801) 天津市科学技术委员会基金资助项目(项目编号:06YFJMJC08300)
关键词 卵巢肿瘤 免疫组织化学 疾病模型 动物 新血管形成 肿瘤坏死因子超家族-15 ovarian neoplasms carcinoma immunohistochemistry disease models, animal neovascularization TNFSF 15
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参考文献6

  • 1Delli Carpini J, Karam AK, Montgomery L. Vascular endothelial growth factor and its relationship to the prognosis and treatment of breast, ovarian, and cervical cancer[J]. Angiognnesis ,2010, 13 (1): 43-58.
  • 2Zhang N, Sanders A J, Ye L,et al.Vascular endothelial growth inhibitor, expression in human prostate cancer tissue and the impact on adhesion and migration of prostate cancer cells in vitro [J].Int J Oncol, 2009,35(6):1473-1480.
  • 3Janat-Amsbury MM, Yockman JW, Anderson ML, et al.Comparison of ID8 MOSE and VEGF-modified ID8 cell lines in an immunocompetent animal model for human ovarian cancer [J]. Anticancer Res,2006,26 (4B):2785-2789.
  • 4Zhai Y. Ni J, Jiang GW, et aI.VEGI, a novel cytokine of the tumor necrosis factor family, is an angiogenesis inhibitor that suppresses the growth of colon carcinomas in vivo[J]. FASEB,1999,13 (1):181- 189.
  • 5Zhang N, Sanders A J, Ye L, et al.Expression of vascular endothelial growth inhibitor (VEGI) in human urothelial cancer of the bladder and its effects on the adhesion and migration of bladder cancer cells in vitro [J]. Anticancer Res ,2010,30 (1):87-95.
  • 6Hanahan D,Folkman J.Patterns and emerging mechanisms of the angiogenic switch during tumorigenesis [J]. Cell, 1996,86 (3):353- 364.

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