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目的探讨Fas/FasL凋亡途径在5-氟尿嘧啶(5-FU)诱导的肾癌细胞凋亡中的作用。方法运用Western blot及TUNEL、MTT技术,检测肾癌细胞株786-0在化疗药物5-FU作用下Fas、FasL的表达变化,分析5-FU、抗Fas单抗CH11、中和性抗FasL单抗NOK-2对癌细胞凋亡与增殖活性的影响。结果Fas、FasL蛋白产物在786-0中均有表达,不同浓度5-FU作用后,中等剂量5-FU70μg/ml作用肾癌细胞株48h时Fas、FasL的表达最显著;786-0在化疗药物5-FU作用下,细胞增殖活性显著降低,细胞凋亡指数显著增加;抗Fas单抗CH11作用于786-0后,细胞凋亡指数显著增加,增殖活性显著降低;CH11与5-FU共同作用于786-0细胞可显著抑制细胞增殖,诱导细胞凋亡;抗FasL单抗NOK-2阻断786-0FasL与Fas相互作用后,细胞的凋亡指数及增殖活性均无显著变化。结论5-FU诱导肾癌细胞凋亡可能不依赖于Fas/FasL凋亡途径。
Objective To investigate the role of Fas / FasL pathway in the apoptosis of renal cell carcinoma induced by 5-fluorouracil (5-FU). Methods Western blot, TUNEL and MTT were used to detect the expression of Fas and FasL in renal cancer cell line 786-0 under the chemotherapeutic drug 5-FU. The effects of 5-FU, anti-Fas monoclonal antibody CH11, neutralizing anti-FasL single Effect of anti-NOK-2 on apoptosis and proliferation of cancer cells. Results The Fas and FasL protein products were expressed in 786-0 cells. The expression of Fas and FasL was significantly higher in the medium-dose of 5-FU 70μg / ml 48h after different concentrations of 5-FU, Under the action of 5-FU, the cell proliferation activity was significantly decreased and the apoptosis index was significantly increased. The apoptosis index of 786-0 was significantly increased by anti-Fas monoclonal antibody CH11, and the proliferation activity was significantly decreased. CH11 and 5-FU Effect of anti-FasL monoclonal antibody NOK-2 on the interaction of 786-0 FasL with Fas did not change the apoptosis index and proliferation activity of 786-0 cells significantly. Conclusion 5-FU-induced apoptosis of renal cell carcinoma may not depend on the Fas / FasL apoptotic pathway.