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作 者:刘畅[1] 徐玉杰[1] 曹亮[1] 方大钊[1] 丁涟沭[1]
机构地区:[1]南京医科大学附属淮安第一医院,江苏淮安223300
出 处:《现代肿瘤医学》2018年第5期664-667,共4页Journal of Modern Oncology
基 金:淮安市科技局科技计划立项(编号:HAS2015018)
摘 要:目的:探究NF-κB抑制剂QNZ对人胶质瘤细胞系U251生物学功能的影响。方法:胶质瘤U251细胞中加入QNZ处理,用CCK8法、Transwell实验、流式细胞术和Western blot检测细胞增殖、侵袭、凋亡以及Caspase-3的表达。结果:QNZ处理后绘制出生长曲线,发现胶质瘤细胞增殖受到抑制。QNZ降低U251细胞的侵袭性。不同浓度QNZ处理后,U251细胞凋亡增加,与QNZ浓度有相关性。QNZ处理后细胞周期被阻滞于G2期。结论:QNZ抑制胶质瘤细胞U251的增殖和细胞侵袭力,促进凋亡并阻滞细胞周期进展,为胶质瘤治疗提供新的思路。Objective:To study the effects of a NF - kB inhibitor QNZ on the proliferation, apoptosis, invasion and cycle of human glioma U251 cells in vitro. Methods: The inhibitory effect of QNZ on cell proliferation was examined by CCK8(cell counting kit 8). The invasion ability was evaluated by Transwell assay. Flow cytometry was used to de-tect the cell cycle distribution and apoptosisrate of U251 cells induced by QNZ. Western blot assay was used to detect the expression of Caspase -3 in different groups. Results: QNZ inhibited the proliferation of U251. QNZ promoted ap-optosis of U251 cells, and the degree of apoptosis was more obvious with the increase of QNZ concentration. After QNZ treatment for 12 hours, apoptosis was detected by flow cytometry. The apoptosis rate of the experimental group was signifcantly increased. The expression of apoptosis related protein Caspase -3 was increased. After treatment with QNZ, the cell cycle was blocked in the G2 phase. Conclusion: QNZ can inhibit the proliferation, promote apoptosis, inhibit the ability of invasion and block cell cycle progression of U251 in glioma cells. It provides a new approach for the treatment of glioma.
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