摘要
目的探究组蛋白去乙酰化酶1(histone deacetylase-1,HDAC1)调节垂体瘤中细胞凋亡的作用机制。方法人垂体瘤细胞系RC-4B/C分为4组,即control组、mimic组、mimic+HDAC1组和HDAC1组。所有细胞按照分组分别通过质粒转染技术上调miR-513c-5p或/和HDAC1的水平;对照组转染等量的NC质粒。通过Starbase预测和双荧光酶素报告验证HDAC1受到miR-513c-5p的靶向调节。检测和比较各组的细胞的细胞生长和调往率,并比较各组细胞miR-513c-5p、HDAC1和PI3K/AKT通路的水平。结果与对照组比较,mimic组的细胞活力降低(P<0.05)。HDAC1组的细胞活力高于对照组(P<0.05),并且mimic+HDAC1组的细胞活力高于mimic组(P<0.05)。mimic组的细胞凋亡率高于对照组(P<0.05)。HDAC1组的细胞凋亡率低于对照组(P<0.05),并且mimic+HDAC1组的细胞凋亡率低于mimic组(P<0.05)。Mimic组的HDAC1的mRNA和蛋白水平低于对照组(P<0.05),并且Mimic+HDAC1组的HDAC1的mRNA和蛋白水平显著高于Mimic组(P<0.05)。MiR-513c-5p直接靶向HDAC1。Mimic组的PI3K、AKT1蛋白表达水平下调(P<0.05),HDAC1组的PI3K、AKT1蛋白蛋白表达水平高于对照组(P<0.05),并且mimic+HDAC1组的PI3K、AKT1蛋白表达水平高于mimic组(P<0.05)。结论HDAC1具有通过调节PI3K/AKT通路促进垂体瘤细胞在增殖和促进凋亡的作用,并且HDAC1对垂体瘤细胞的促癌作用受到miR-513c-5p的靶向调控。
Objective To explore the mechanism of action of histone deacetylase-1(HDAC1)in regulating apoptosis in pituitary tumors.Methods The human pituitary tumor cell line RC-4 B/C was divided into 4 groups,namely control group,mimic group,mimic+HDAC1 group and HDAC1 group.All cells were up-regulated by plasmid transfection techniques to miR-513 c-5 p or/and HDAC1 levels;the control group was transfected with the same amount of NC plasmid.HDAC1 was confirmed to be targeted by miR-513 c-5 p by Starbase prediction and dual luciferase reporter.The cell growth and rate of cells in each group were examined and compared,and the levels of miR-513 c-5 p,HDAC1 and PI3 K/AKT pathways in each group were compared.Results Compared with the control group,the cell viability of the mimic group was decreased(P<0.05).The cell viability of the HDAC1 group was higher than that of the control group(P<0.05),and the cell viability of the mimic+HDAC1 group was higher than that of the mimic group(P<0.05).The apoptosis rate of the mimic group was higher than that of the control group(P<0.05).The apoptosis rate of HDAC1 group was lower than that of the control group(P<0.05),and the apoptosis rate of mimic+HDAC1 group was lower than that of mimic group(P<0.05).The mRNA and protein levels of HDAC1 in the Mimic group were lower than those in the control group(P<0.05),and the mRNA and protein levels of HDAC1 in the Mimic+HDAC1 group were significantly higher than those in the Mimic group(P<0.05).MiR-513 c-5 p directly targets HDAC1.The expression levels of PI3 K and AKT1 protein in Mimic group were down-regulated(P<0.05).The expression levels of PI3 K and AKT1 protein in HDAC1 group were higher than those in control group(P<0.05),and the expression levels of PI3 K and AKT1 in mimic+HDAC1 group were higher than mimic.Group(P<0.05).Conclusion HDAC1 has a role in promoting proliferation and promoting apoptosis of pituitary tumor cells by modulating the PI3 K/AKT pathway,and the cancer-promoting effect of HDAC1 on pituitary tumor cells is regulated by miR-513 c-5 p.
作者
王剑
韩书清
周晓飞
Wang Jian;Han Shuqing;Zhou Xiaofei(Department of Neurosurgery,Wuhan Red Cross Hospital,Wuhan,430000)
出处
《立体定向和功能性神经外科杂志》
2020年第4期213-217,共5页
Chinese Journal of Stereotactic and Functional Neurosurgery
作者简介
通讯作者:韩书清,shu_8253624@163.com
