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背景与目的:胶质瘤干细胞(glioma stem cell,GSC)在胶质瘤发展及治疗抗拒中发挥重要作用。我们以往的研究表明,新型STAT3信号转导通路抑制剂(STAT3 inhibitor,STI)WP1193能够诱导GSC产生细胞周期阻滞及凋亡。本研究旨在探讨STI是否能在体外诱导GSC产生自噬现象。方法:从手术切除的胶质母细胞瘤中分离及培养GSC。使用STI处理GSC。利用细胞计数法检测STI对GSC增殖的影响。使用Western blot检测自噬相关蛋白LC3的表达情况。吖啶橙染色后,利用荧光显微镜及流式细胞技术检测酸性自噬小体。使用透射电镜检测GSC中自噬小体。结果:STI剂量依赖性的抑制GSC的增殖。STI处理后,GSC中出现LC3表达的切换。STI处理后,GSC中出现自噬小体,且出现自噬小体细胞的比例增加。结论:STI能够在GSC中诱导自噬现象的产生。自噬在STI治疗中的意义及调节机制需要进一步的研究。
BACKGROUND & AIM: Glioma stem cells (GSCs) play an important role in glioma development and therapeutic resistance. Our previous studies showed that STAT11 inhibitor (STAT) inhibitor WP1193 can induce cell cycle arrest and apoptosis in GSCs. This study aimed to investigate whether STI can induce autophagy in GSCs in vitro. Methods: GSC was isolated and cultured from surgically removed glioblastoma. Use STI to process GSC. The effect of STI on the proliferation of GSC was detected by cytometry. Western blot was used to detect the expression of autophagy-related protein LC3. Acridine orange staining, the use of fluorescence microscopy and flow cytometry to detect acidic autophagy bodies. Transmission electron microscopy was used to detect autophagosomes in GSC. Results: STI dose-dependently inhibited the proliferation of GSC. After STI treatment, switching of LC3 expression occurred in GSC. After STI treatment, autophagosomes appeared in GSC, and the proportion of autophagy somatic cells increased. Conclusion: STI can induce autophagy in GSCs. The significance and regulatory mechanism of autophagy in STI treatment need further study.