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目的:研究酪氨酸激酶抑制剂(STI571)对恶性胶质瘤细胞的肿瘤生物学调节作用。方法:用免疫组化法探查血小板源生长因子(PDGF)及其受体在T98G,U87MG,LNZ308,RG四种胶质瘤细胞的表达;MTT法用于检查STI571/TMZ单独或联合应用对胶质瘤细胞的增殖抑制作用,STI571诱导的细胞凋亡途径由流式细胞仪检测,免疫印迹杂交法用来探查STI571抵抗细胞的蛋白激酶网络变化。结果:所用胶质瘤细胞均不同程度的表达PDGF及受体。STI571与TMZ相互协同作用于胶质瘤细胞株T98G;10滋mol/LSTI571可部分抑制所测胶质瘤细胞增殖、可完全抑制其形成集落;高于10滋mol/L浓度的STI571可快速诱导胶质瘤细胞凋亡或坏死;胶质瘤细胞株T98G与STI571长期共培养后,瘤细胞蛋白激酶网络有较大改变。结论:研究表明,PDGF受体酪氨酸激酶抑制剂STI571有较强的抑制恶性胶质瘤细胞(GBM)增殖的作用并可能与其他化疗药物协同抗肿瘤。
AIM: To investigate the tumorigenicity of tyrosine kinase inhibitor (STI571) in malignant glioma cells. Methods: The expression of platelet-derived growth factor (PDGF) and its receptor in four glioma cells T98G, U87MG, LNZ308 and RG were detected by immunohistochemistry. MTT assay was used to examine the effect of STI571 / TMZ alone or in combination STI571-induced apoptosis was detected by flow cytometry, and Western blot hybridization was used to investigate STI571-resistant protein kinase network changes. Results: The glioma cells used to express PDGF and its receptors to different degrees. STI571 and TMZ mutually synergistically act on glioma cell line T98G; 10μmol / L LSTI571 can partially inhibit the proliferation of glioma cells and inhibit the formation of colonies completely; STI571 at a concentration higher than 10μmol / L can be rapidly induced Glioma cell apoptosis or necrosis; glioma cell line T98G and STI571 long-term co-culture, the tumor cell protein kinase network have a greater change. Conclusion: PDGF receptor tyrosine kinase inhibitor STI571 has a strong inhibitory effect on the proliferation of glioblastoma cells (GBM) and may be synergistic with other chemotherapy drugs in anti-tumor.