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1An ATF24 peptide-functionalized β-elemene-nanostructured lipid carrier combined with cisplatin for bladder cancer treatment显示文摘Objective:In this study,we aimed to develop an amino-terminal fragment(ATF)peptide-targeted liposome carryingβ-elemene(ATF24-PEG-Lipo-β-E)for targeted delivery into urokinase plasminogen activator receptor-overexpressing bladder cancer cells combined with cisplatin(DDP)for bladder cancer treatment.Methods:The liposomes were prepared by ethanol injection and high-pressure microjet homogenization.The liposomes were characterized,and the drug content,entrapment efficiency,andin vitro release were studied.The targeting efficiency was investigated using confocal microscopy,ultra-fast liquid chromatography,and an orthotopic bladder cancer model.The effects of ATF24-PEG-Lipo-β-E combined with DDP on cell viability and proliferation were evaluated by a Cell Counting Kit-8(CCK-8)assay,a colony formation assay,and cell apoptosis and cell cycle analyses.The anticancer effects were evaluated in a KU-19-19 bladder cancer xenograft model.Results:ATF24-PEG-Lipo-β-E had small and uniform sizes(~79 nm),high drug loading capacity(~5.24 mg/mL),high entrapment efficiency(98.37±0.95%),and exhibited sustained drug release behavior.ATF24-PEG-Lipo-β-E had better targeting efficiency and higher cytotoxicity than polyethylene glycol(PEG)ylatedβ-elemene liposomes(PEG-Lipo-β-E).DDP,combined with ATF24-PEG-Lipo-β-E,exerted a synergistic effect on cellular apoptosis and cell arrest at the G2/M phase,and these effects were dependent on the caspase-dependent pathway and Cdc25C/Cdc2/cyclin B1 pathways.Furthermore,thein vivo antitumor activity showed that the targeted liposomes effectively inhibited the growth of tumors,using the combined strategy.Conclusions:The present study provided an effective strategy for the targeted delivery ofβ-elemene(β-E)to bladder cancer,and a combined strategy for bladder cancer treatment.Bingtao Zhai Peng Chen Wengang Wang Shuiping Liu Jiao Feng Ting Duan Yu Xiang Ruonan Zhang Mingming Zhang Xuemeng Han Xiaying Chen Qiujie Li Guohua Li Ying Liu Xingxing Huang Wenzheng Zhang Ting Pan Lili Yan Ting Jin Tian Xie Xinbing Sui 2020Cancer Biology & Medicine2020,17,3:5
2替米沙坦通过Wnt/β-catenin信号通路影响非小细胞肺癌A549细胞增殖、迁移和凋亡的研究显示文摘目的研究替米沙坦对非小细胞肺癌A549细胞增殖、迁移和凋亡的影响,并探讨其机制。方法体外培养非小细胞肺癌细胞株A549,采用CCK-8法检测不同浓度替米沙坦对A549细胞增殖活性的影响,以克隆形成实验检测不同浓度替米沙坦处理下A549的存活分数,以划痕实验检测不同浓度替米沙坦对A549细胞迁移能力的影响,Hoechst染色检测不同浓度替米沙坦对A549凋亡的影响,用Western blotting检测β-肌动蛋白(β-actin)、增殖细胞核抗原(PCNA)、Bax、Bcl-2、Wnt-3a、β-连环蛋白(β-catenin)、丝氨酸蛋白激酶3β(p-GSK-3β)、糖原合成酶激酶-3β(GSK-3β)、c-myc等蛋白的表达。结果不同浓度替米沙坦处理抑制了A549细胞增殖活性、克隆形成率和迁移,减少PCNA表达,并且存在浓度依赖性。替米沙坦处理促进了A549细胞的凋亡,显著增加促凋亡蛋白Bax和减少抗凋亡蛋白Bcl-2的表达。替米沙坦处理后A549细胞的Wnt-3a、β-catenin、c-myc、p-GSK-3β的表达减少,GSK-3β的表达增加。结论替米沙坦可能在非小细胞肺癌A549细胞的增殖、迁移和凋亡中起到作用,抑制Wnt/β-catenin信号通路可能是其中的一个机制。王灵杰 赵懂华 黄章锋 李蒙君 国鹏飞 王勇杰 2022中国胸心血管外科临床杂志2022,29,1:3
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