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目的研究BAFF对Raji细胞促增殖作用的机制,分析其对非经典NF-κBB信号途径的调节作用,并初步探讨RIPK2与BAFF/BAFF-R介导的信号通路的相关性。方法以不同浓度重组人BAFF刺激Raji细胞,MTT法分析BAFF对Raji细胞的促增殖作用,应用实时荧光定量PCR(real time q-PCR)与蛋白质印迹实验(Western blotting)检测Raji细胞中BAFF、BAFF-R、NIK、p52、Bcl-XL及RIPK2的表达。结果 BAFF能促进Raji细胞的增殖,且具有明显的剂量效应与时间效应依赖关系;BAFF、BAFF-R、NIK、p52、Bcl-XL及RIPK2在mRNA及蛋白水平的表达均随重组人BAFF浓度的增加而升高(P<0.05)。结论重组人BAFF刺激Raji细胞后能激活非经典NF-κB信号途径,并引起下游靶蛋白Bcl-XL等抗凋亡因子的过表达,促进肿瘤细胞的存活和增殖。BAFF可以上调RIPK2的表达,提示RIPK2与非经典NF-κB信号途径之间可能存在功能联系。
OBJECTIVE: To study the mechanism of BAFF on the proliferation of Raji cells and its regulation on the non-canonical NF-κB signaling pathway, and to explore the relationship between RIPK2 and BAFF / BAFF-R signaling pathway. Methods Raji cells were stimulated with recombinant human BAFF at different concentrations. The effect of BAFF on the proliferation of Raji cells was analyzed by MTT assay. The effects of BAFF, BAFF and Raji cells were detected by real time q-PCR and Western blotting. -R, NIK, p52, Bcl-XL and RIPK2 expression. BAFF, BAFF-R, NIK, p52, Bcl-XL and RIPK2 mRNA and protein levels were all increased with the concentration of recombinant human BAFF Increased and increased (P <0.05). Conclusion Recombinant human BAFF can stimulate non-canonical NF-κB signal pathway after stimulating Raji cells and induce the overexpression of anti-apoptotic factors such as Bcl-XL and promote the survival and proliferation of tumor cells. BAFF can up-regulate the expression of RIPK2, suggesting that there may be a functional relationship between RIPK2 and non-classical NF-κB signaling pathway.