let-7f转染非小细胞肺癌癌症对候选靶基因的调控作用

Q2 Biochemistry, Genetics and Molecular Biology
V. Zafari, M. Asadi, Nasim Bakhtiyari, Mahsa Sadeghzadeh, M. Khalili, H. Zarredar, Soghra Bornehdeli, E. Seyedrezazadeh
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引用次数: 1

摘要

背景:Let-7f对生物过程具有重要影响;然而,其在癌症发病机制中的生物学和分子功能尚不清楚。我们旨在研究let-7f及其候选靶基因在癌症组织和A549细胞系中的表达水平。方法:首先利用生物信息学数据库筛选let-7f的候选靶基因。然后,使用定量实时PCR和Western印迹法测量let-7f及其靶基因(包括HMGA2、ARID3B、SMARCAD1和FZD3)在非小细胞肺癌癌症(NSCLC)患者的肺组织和A549细胞系中的相对基因和蛋白质表达。采用电穿孔法用let-7f模拟物和microRNA抑制剂转染A549细胞。用MTT法评估let-7f转染对A549细胞活力的影响。结果:let-7f-5p的表达水平在NSCLC患者中显著下调(p=0.0013),HMGA2和FZD3的表达水平显著上调(p<0.05)。在A549细胞中,用let-7f模拟物转染后,HMGA1、ARID3B、SMARCAD1和FZD3 mRNA和蛋白水平均下降。此外,let-7f的过表达显著抑制了A549细胞的增殖和活力(p=0.017)。结论:let-7f和HMGA2作为NSCLC的生物标志物具有很高的价值。let-7f作为一种主要的肿瘤抑制调节因子,通过直接靶向基因(如HMGA2)抑制癌症细胞的生存能力和增殖,并可作为NSCLC早期诊断的标志物。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Regulatory Effect of let-7f Transfection in Non-Small Cell Lung Cancer on its Candidate Target Genes
Background: Let-7f has essential impacts on biological processes; however, its biological and molecular functions in lung cancer pathogenesis have yet been remained unclear. We aimed to investigate the expression level of let-7f and its candidate target genes both in lung cancer tissues and A549 cell line. Methods: Bioinformatics databases were first used to select candidate target genes of let-7f. Then the relative gene and protein expressions of let-7f and its target genes, including HMGA2, ARID3B, SMARCAD1, and FZD3, were measured in lung tissues of Non-Small Cell Lung Cancer (NSCLC) patients and A549 cell line using quantitative real-time PCR and Western blotting. The electroporation method was used to transfect A549 cells with let-7f mimic and microRNA inhibitor. The impact of let-7f transfection on the viability of A549 cells was assessed using MTT assay. The expression data of studied genes were analyzed statistically Results: Results indicated significant downregulated expression level of let-7f-5p (p = 0.0013) and upregulated level of the HMGA2 and FZD3 in NSCLC cases (p < 0.05). In A549 cells, after transfection with let-7f mimic, the expression of both mRNA and protein levels of HMGA2, ARID3B, SMARCAD1, and FZD3 decreased. Also, the overexpression of let-7f significantly inhibited the A549 cell proliferation and viability (p = 0.017). Conclusion: Our findings exhibited the high value of let-7f and HMGA2 as biomarkers for NSCLC. The let-7f, as a major tumor suppressor regulatory factor via direct targeting genes (e.g. HMGA2), inhibits lung cancer cell viability and proliferation and could serve as a marker for the early diagnostic of NSCLC.
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来源期刊
Iranian Biomedical Journal
Iranian Biomedical Journal Biochemistry, Genetics and Molecular Biology-Biochemistry, Genetics and Molecular Biology (all)
CiteScore
3.20
自引率
0.00%
发文量
42
审稿时长
8 weeks
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