Beclin1基因在SW620细胞自噬和凋亡中作用

发布时间：2018-03-16 06:19

本文选题：结直肠癌　切入点：Beclin　出处：《南方医科大学学报》2017年03期 　论文类型：期刊论文

【摘要】：目的探讨Beclin1基因在SW620细胞自噬和凋亡中作用。方法采用RNA干扰技术抑制Beclin1表达,Beclin1被抑制后细胞的存活能力通过MTT实验评估;结直肠癌细胞SW620在血清剥夺状态下自噬活性通过LC3蛋白水平评估;分别经血清剥夺、星孢菌素及依托泊苷处理的SW620凋亡率通过流式细胞仪检测;Beclin1表达情况经Western blot评估。结果 pSUPERBecl组细胞血清剥夺后存活能力显著降低(P0.05),在血清剥夺24 h后,空白对照组和p SUPER-non组抗凋亡能力比p SUPERBecl组更强(P0.05),星孢菌素处理后,pSUPER-Becl组细胞凋亡最为显著(P0.05),用依托泊苷处理后得到相似的结果(P0.05);pSUPER-non组与空白对照组细胞中Beclin1的表达随血清剥夺时间的延长呈现上调趋势(P0.05),这与LC3的表达变化相一致;而pSUPER-Becl组LC3的表达显著减少(P0.05)。结论 Beclin1是结直肠癌细胞中自噬和凋亡的关键调节因素,并且维持凋亡和自噬的平衡;Beclin1通过调节细胞自噬活性,在结直肠癌发展与演进中作为一种保护机制,使肿瘤细胞免受到低营养和化疗所致的损伤而持续生存。
[Abstract]:Objective to investigate the role of Beclin1 gene in autophagy and apoptosis of SW620 cells. Methods RNA interference technique was used to inhibit the viability of SW620 cells after Beclin1 expression was inhibited by MTT assay. The autophagy activity of colorectal cancer cell SW620 was evaluated by the level of LC3 protein in the state of serum deprivation. The apoptotic rate of SW620 treated with astrocystin and etoposide was evaluated by Western blot by flow cytometry. Results in pSUPERBecl group, the viability of pSUPERBecl cells was significantly decreased after serum deprivation, and 24 h after serum deprivation. The anti-apoptotic ability of blank control group and pSUPER-non group was stronger than that of p SUPERBecl group, and the apoptosis of pSUPER-Becl group was the most significant after treatment with astrocystin. Similar results were obtained by etoposide treatment with Beclin1 expression in P0.05PSUPER-non group and blank control group. The prolongation of serum deprivation time showed an upward trend of P0.05, which was consistent with the change of LC3 expression. Conclusion Beclin1 is the key regulator of autophagy and apoptosis in colorectal cancer cells, and maintains the balance between apoptosis and autophagy by regulating autophagy activity. As a protective mechanism in the development and progression of colorectal cancer, tumor cells continue to survive from low nutrition and chemotherapy-induced damage.
【作者单位】：锦州医科大学研究生学院;锦州医科大学附属第一医院大肠外科;
【基金】：辽宁省教育厅科学技术一般项目(L2014333)
【分类号】：R730.2

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