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超声靶向微泡破坏介导的miR-767抑制可抑制非小细胞肺癌的肿瘤进展。

Ultrasound-targeted microbubble destruction-mediated miR-767 inhibition suppresses tumor progression of non-small cell lung cancer.

作者信息

Li Xiaohua, Xu Min, Lv Wenyu, Yang Xingwang

机构信息

Department of Ultrasonography, Zibo City Linzi District People's Hospital, Zibo, Shandong 255400, P.R. China.

Department of Pediatric Surgery, Burns and Plastic Surgery, and Hemorrhoids Fistula Surgery, Yidu Central Hospital of Weifang, Shandong 262500, P.R. China.

出版信息

Exp Ther Med. 2020 May;19(5):3391-3397. doi: 10.3892/etm.2020.8602. Epub 2020 Mar 12.

Abstract

MicroRNAs (miRNAs/miRs) have important roles in tumor progression in various human cancers. Ultrasound-targeted microbubble destruction (UTMD)-mediated gene transfection has been considered a useful tool for improving cancer treatment. The present study aimed to investigate the role of miR-767 in non-small cell lung cancer (NSCLC) and further analyze the effects of UTMD-mediated miR-767 inhibition on tumor progression. The expression of miR-767 was measured by reverse transcription-quantitative PCR. UTMD-mediated miR-767 inhibition was achieved by the co-transfection of microbubbles and miR-767 inhibitor in NSCLC cells. Cell proliferation was assessed by a CCK-8 assay and cell migration and invasion were examined by a Transwell assay. The expression of miR-767 was increased in NSCLC serum, tissues and cells compared with controls. The reduction of miR-767 in NSCLC cells led to the inhibition of cell proliferation, migration and invasion. UTMD increased the transfection efficiency of the miR-767 inhibitor in NSCLC cells, and UTMD-mediated miR-767 inhibition resulted in a more significant suppressive effect on tumor cell proliferation, migration and invasion. Taken together, the results indicated that miR-767 expression is upregulated in both NSCLC clinical samples and cells. The downregulation of miR-767 can inhibit tumor cell proliferation, migration and invasion, and these effects are further promoted by UTMD-mediated miR-767 inhibition, which indicated the potential of a UTMD-mediated miR-767 inhibition as a novel therapeutic strategy for NSCLC treatment.

摘要

微小RNA(miRNAs/miRs)在多种人类癌症的肿瘤进展中发挥着重要作用。超声靶向微泡破坏(UTMD)介导的基因转染被认为是改善癌症治疗的一种有用工具。本研究旨在探讨miR-767在非小细胞肺癌(NSCLC)中的作用,并进一步分析UTMD介导的miR-767抑制对肿瘤进展的影响。通过逆转录定量PCR检测miR-767的表达。在NSCLC细胞中,通过微泡与miR-767抑制剂共转染实现UTMD介导的miR-767抑制。通过CCK-8法评估细胞增殖,通过Transwell法检测细胞迁移和侵袭。与对照组相比,NSCLC血清、组织和细胞中miR-767的表达增加。NSCLC细胞中miR-767的降低导致细胞增殖、迁移和侵袭受到抑制。UTMD提高了miR-767抑制剂在NSCLC细胞中的转染效率,并且UTMD介导的miR-767抑制对肿瘤细胞增殖、迁移和侵袭产生了更显著的抑制作用。综上所述,结果表明miR-767在NSCLC临床样本和细胞中均上调。miR-767的下调可抑制肿瘤细胞增殖、迁移和侵袭,并且UTMD介导的miR-767抑制进一步促进了这些作用,这表明UTMD介导的miR-767抑制作为NSCLC治疗的一种新的治疗策略具有潜力。

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