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
{"title":"let-7f转染非小细胞肺癌癌症对候选靶基因的调控作用","authors":"V. Zafari, M. Asadi, Nasim Bakhtiyari, Mahsa Sadeghzadeh, M. Khalili, H. Zarredar, Soghra Bornehdeli, E. Seyedrezazadeh","doi":"10.52547/ibj.26.3.209","DOIUrl":null,"url":null,"abstract":"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.","PeriodicalId":14500,"journal":{"name":"Iranian Biomedical Journal","volume":null,"pages":null},"PeriodicalIF":0.0000,"publicationDate":"2022-04-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"1","resultStr":"{\"title\":\"Regulatory Effect of let-7f Transfection in Non-Small Cell Lung Cancer on its Candidate Target Genes\",\"authors\":\"V. Zafari, M. Asadi, Nasim Bakhtiyari, Mahsa Sadeghzadeh, M. Khalili, H. Zarredar, Soghra Bornehdeli, E. Seyedrezazadeh\",\"doi\":\"10.52547/ibj.26.3.209\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"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.\",\"PeriodicalId\":14500,\"journal\":{\"name\":\"Iranian Biomedical Journal\",\"volume\":null,\"pages\":null},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2022-04-27\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"1\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Iranian Biomedical Journal\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.52547/ibj.26.3.209\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q2\",\"JCRName\":\"Biochemistry, Genetics and Molecular Biology\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Iranian Biomedical Journal","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.52547/ibj.26.3.209","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q2","JCRName":"Biochemistry, Genetics and Molecular Biology","Score":null,"Total":0}
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.
求助全文
通过发布文献求助,成功后即可免费获取论文全文。 去求助
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
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
确定
请完成安全验证×
copy
已复制链接
快去分享给好友吧!
我知道了
右上角分享
点击右上角分享
0
联系我们:info@booksci.cn Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。 Copyright © 2023 布克学术 All rights reserved.
京ICP备2023020795号-1
ghs 京公网安备 11010802042870号
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术官方微信