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MicroRNA-30c inhibits pancreatic cancer cell proliferation by targeting twinfilin 1 and indicates a poor prognosis 被引量:2
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作者 Lu-Lu Sun Ming Cheng Xiao-Dong Xu 《World Journal of Gastroenterology》 SCIE CAS 2019年第42期6311-6321,共11页
BACKGROUND Studies have reported that microRNA-30c(miR-30c)has vital functions in the development and progression of multiple cancers.AIM To investigate the clinical significance and role of miR-30c in pancreatic canc... BACKGROUND Studies have reported that microRNA-30c(miR-30c)has vital functions in the development and progression of multiple cancers.AIM To investigate the clinical significance and role of miR-30c in pancreatic cancer.METHODS MiR-30c and twinfilin 1(TWF1)expression levels were analyzed in Gene Expression Omnibus datasets and validated in human pancreatic cancer by quantitative real-time polymerase chain reaction(RT-qPCR).The effects of miR-30c on pancreatic cancer cell growth,apoptosis,and cell cycle were evaluated by CCK-8 and flow cytometry assays.Furthermore,the in vivo effects were investigated using a subcutaneous xenograft experiment.Target gene prediction software and luciferase reporter assays were used to identify TWF1 as a direct target of miR-30c.RESULTS The expression of miR-30c was significantly decreased in pancreatic cancer tissues and associated with survival.Gain-and loss-of-function assays showed that miR-30c suppressed pancreatic cancer cell proliferation in vitro and in vivo.RT-qPCR,Western blot,and luciferase reporter assays showed that miR-30c directly targeted TWF1.The expression level of miR-30c was negatively correlated with TWF1 expression in pancreatic cancer tissues.Furthermore,the effects of ectopic miR-30c were rescued by TWF1 overexpression.CONCLUSION Our results identified the role of the miR-30c/TWF1 axis in pancreatic cancer progression and demonstrated that miR-30c might serve as a prognostic biomarker and therapeutic target for pancreatic cancer. 展开更多
关键词 PANCREATIC cancer MicroRNA-30c PROLIFERATION twinfilin 1
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Twinfilin-1过表达缓解镉诱导肾细胞重金属中毒及凋亡 被引量:1
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作者 郭艳红 吴琴宁 +1 位作者 邓权 周强 《西部医学》 2022年第4期520-524,共5页
目的探究细胞骨架调控蛋白Twinfilin-1过表达对镉诱导肾细胞重金属中毒及凋亡的影响。方法体外培养猪肾细胞LLC-PK1,随机分为对照组、模型组、模型+pc DNA空载体组、模型+Twinfilin-1过表达组,以8μmol/L镉处理细胞24 h建立重金属中毒... 目的探究细胞骨架调控蛋白Twinfilin-1过表达对镉诱导肾细胞重金属中毒及凋亡的影响。方法体外培养猪肾细胞LLC-PK1,随机分为对照组、模型组、模型+pc DNA空载体组、模型+Twinfilin-1过表达组,以8μmol/L镉处理细胞24 h建立重金属中毒模型。采用实时荧光PCR技术和蛋白印迹实验检测Twinfilin-1的表达,CCK8实验检测细胞增殖,流式细胞术检测细胞凋亡和线粒体膜电位的变化,蛋白印迹检测凋亡相关蛋白[B淋巴细胞瘤-2(Bcl-2)、Bcl-2相关X蛋白(Bax)、半胱氨酸天冬氨酸特异性蛋白酶(Caspase3、9)]水平。结果与对照组比较,模型组Twinfilin-1 mRNA及蛋白水平、细胞增殖能力、线粒体膜电位降低,细胞凋亡率、Bax/Bcl-2、cleaved cas9/cas9及cleaved cas3/cas3水平增加(P<0.05);与模型组比较,模型+Twinfilin-1过表达组Twinfilin-1 mRNA及蛋白水平、细胞增殖能力、线粒体膜电位增加,细胞凋亡率、Bax/Bcl-2、cleaved cas9/cas9及cleaved cas3/cas3水平降低(P<0.05),而模型组+pc DNA空载体组无明显变化(P>0.05)。结论Twinfilin-1过表达可能通过下调凋亡关键因子Bax/Bcl-2水平,抑制Caspase3、9的活化,减少细胞凋亡,维持正常线粒体膜电位,从而保护镉诱导肾细胞重金属中毒。 展开更多
关键词 twinfilin-1 肾细胞 重金属中毒 凋亡 线粒体损伤
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Twinfilin-1基因对H9C2心肌细胞凋亡和增殖的影响
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作者 艾克热木·吐尔逊 《中西医结合心脑血管病杂志》 2020年第23期3963-3967,共5页
目的探究Twinfilin-1(Twf-1)基因对H9C2心肌细胞凋亡和增殖的影响。方法构建Twf-1 siRNA、pCXN2-Flag空质粒、pCXN2-Flag-h Twf-1过表达质粒,将实验用H9C2心肌细胞分为5组,即空白对照组、阴性对照组、Twf-1沉默组、Twf-1沉默+空质粒组、... 目的探究Twinfilin-1(Twf-1)基因对H9C2心肌细胞凋亡和增殖的影响。方法构建Twf-1 siRNA、pCXN2-Flag空质粒、pCXN2-Flag-h Twf-1过表达质粒,将实验用H9C2心肌细胞分为5组,即空白对照组、阴性对照组、Twf-1沉默组、Twf-1沉默+空质粒组、Twf-1沉默+过表达Twf-1组,分别用空白试剂、Twf-1 siRNA慢病毒、Twf-1 siRNA慢病毒+pCXN2-Flag空质粒、Twf-1 siRNA慢病毒+pCXN2-Flag-h Twf-1过表达质粒转染H9C2心肌细胞。转染72 h后,采用荧光定量聚合酶链式反应(RT-PCR)检测目的基因Twf-1表达情况,采用CCK8检测不同组别心肌细胞增殖情况,采用流式细胞术检测心肌细胞凋亡情况。结果荧光显微镜下可见慢病毒转染48 h后,阴性对照组和Twf-1沉默组80%以上细胞均有绿色荧光标记。与空白对照组和阴性对照组相比,Twf-1沉默组、Twf-1沉默+空质粒组心肌细胞中Twf-1基因的表达水平及细胞增殖率均明显降低(P<0.05),心肌细胞凋亡率均明显增加(P<0.05),Twf-1沉默+过表达Twf-1组心肌细胞中Twf-1基因的表达水平及细胞增殖率则明显增加(P<0.05),其心肌细胞凋亡率与空白对照组和阴性对照组比较无统计学意义,与Twf-1沉默组、Twf-1沉默+空质粒组相比则明显降低,组间差异具有统计学意义(P<0.05)。结论靶向沉默Twf-1基因表达可有效抑制心肌细胞增殖,促进心肌细胞凋亡,过表达Twf-1基因能在一定程度上逆转Twf-1沉默对心肌细胞增殖和凋亡功能的影响。 展开更多
关键词 心肌细胞 凋亡 增殖 twinfilin-1基因
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