预测miR-203a-3p和miR-29a-3p对DNMT3B和GAS7基因表达的可能影响。

IF 1.5 Q3 MATHEMATICAL & COMPUTATIONAL BIOLOGY
Afgar Ali, Sattarzadeh Bardsiri Mahla, Vahidi Reza, Farsinejad Alireza
{"title":"预测miR-203a-3p和miR-29a-3p对DNMT3B和GAS7基因表达的可能影响。","authors":"Afgar Ali,&nbsp;Sattarzadeh Bardsiri Mahla,&nbsp;Vahidi Reza,&nbsp;Farsinejad Alireza","doi":"10.1515/jib-2021-0016","DOIUrl":null,"url":null,"abstract":"<p><p>Aberrant expression of genes involved in methylation, including DNA methyltransferase 3 Beta (<i>DNMT3B</i>), can cause hypermethylation of various tumor suppressor genes. In this regard, various molecular factors such as microRNAs can play a critical role in regulating these methyltransferase enzymes and eventually downstream genes such as growth arrest specific 7 (<i>GAS7</i>). Accordingly, in the present study we aimed to predict regulatory effect of miRNAs on <i>DNMT3B</i> and <i>GAS7</i> genes expression in melanoma cell line. hsa-miR-203a-3p and hsa-miR-29a-3p were predicted and selected using bioinformatics software. The Real-time PCR technique was performed to investigate the regulatory effect of these molecules on the <i>DNMT3B</i> and <i>GAS7</i> genes expression. Expression analysis of <i>DNMT3B</i> gene in A375 cell line showed that there was a significant increase compared to control (<i>p</i> value = 0.0015). Analysis of hsa-miR-203a-3p and hsa-miR-29a-3p indicated the insignificant decreased expression in melanoma cell line compared to control (<i>p</i> value < 0.05). Compared to control, the expression of GAS7 gene in melanoma cells showed a significant decrease (<i>p</i> value = 0.0323). Finally, our findings showed that the decreased expression of hsa-miR-203a-3p and hsa-miR-29a-3p can hypothesize that their aberrant expression caused <i>DNMT3B</i> dysfunction, possible methylation of the <i>GAS7</i> gene, and ultimately decreased its expression. However, complementary studies are necessary to definite comment.</p>","PeriodicalId":53625,"journal":{"name":"Journal of Integrative Bioinformatics","volume":null,"pages":null},"PeriodicalIF":1.5000,"publicationDate":"2021-12-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9069646/pdf/","citationCount":"3","resultStr":"{\"title\":\"Predicting the possible effect of miR-203a-3p and miR-29a-3p on <i>DNMT3B</i> and <i>GAS7</i> genes expression.\",\"authors\":\"Afgar Ali,&nbsp;Sattarzadeh Bardsiri Mahla,&nbsp;Vahidi Reza,&nbsp;Farsinejad Alireza\",\"doi\":\"10.1515/jib-2021-0016\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>Aberrant expression of genes involved in methylation, including DNA methyltransferase 3 Beta (<i>DNMT3B</i>), can cause hypermethylation of various tumor suppressor genes. In this regard, various molecular factors such as microRNAs can play a critical role in regulating these methyltransferase enzymes and eventually downstream genes such as growth arrest specific 7 (<i>GAS7</i>). Accordingly, in the present study we aimed to predict regulatory effect of miRNAs on <i>DNMT3B</i> and <i>GAS7</i> genes expression in melanoma cell line. hsa-miR-203a-3p and hsa-miR-29a-3p were predicted and selected using bioinformatics software. The Real-time PCR technique was performed to investigate the regulatory effect of these molecules on the <i>DNMT3B</i> and <i>GAS7</i> genes expression. Expression analysis of <i>DNMT3B</i> gene in A375 cell line showed that there was a significant increase compared to control (<i>p</i> value = 0.0015). Analysis of hsa-miR-203a-3p and hsa-miR-29a-3p indicated the insignificant decreased expression in melanoma cell line compared to control (<i>p</i> value < 0.05). Compared to control, the expression of GAS7 gene in melanoma cells showed a significant decrease (<i>p</i> value = 0.0323). Finally, our findings showed that the decreased expression of hsa-miR-203a-3p and hsa-miR-29a-3p can hypothesize that their aberrant expression caused <i>DNMT3B</i> dysfunction, possible methylation of the <i>GAS7</i> gene, and ultimately decreased its expression. However, complementary studies are necessary to definite comment.</p>\",\"PeriodicalId\":53625,\"journal\":{\"name\":\"Journal of Integrative Bioinformatics\",\"volume\":null,\"pages\":null},\"PeriodicalIF\":1.5000,\"publicationDate\":\"2021-12-16\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9069646/pdf/\",\"citationCount\":\"3\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Journal of Integrative Bioinformatics\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.1515/jib-2021-0016\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q3\",\"JCRName\":\"MATHEMATICAL & COMPUTATIONAL BIOLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of Integrative Bioinformatics","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1515/jib-2021-0016","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q3","JCRName":"MATHEMATICAL & COMPUTATIONAL BIOLOGY","Score":null,"Total":0}
引用次数: 3

摘要

包括DNA甲基转移酶3 β (DNMT3B)在内的参与甲基化的基因的异常表达可导致多种肿瘤抑制基因的超甲基化。在这方面,各种分子因子如microrna可以在调节这些甲基转移酶以及最终下游基因如生长停滞特异性7 (GAS7)中发挥关键作用。因此,在本研究中,我们旨在预测miRNAs对黑色素瘤细胞系DNMT3B和GAS7基因表达的调控作用。利用生物信息学软件对hsa-miR-203a-3p和hsa-miR-29a-3p进行预测和选择。采用Real-time PCR技术研究这些分子对DNMT3B和GAS7基因表达的调控作用。DNMT3B基因在A375细胞系中的表达分析显示,与对照组相比,DNMT3B基因的表达显著增加(p值= 0.0015)。分析hsa-miR-203a-3p和hsa-miR-29a-3p在黑色素瘤细胞系中的表达与对照组相比,差异不显著(p值< 0.05)。与对照组相比,GAS7基因在黑色素瘤细胞中的表达显著降低(p值= 0.0323)。最后,我们的研究结果表明,hsa-miR-203a-3p和hsa-miR-29a-3p的表达减少可以假设它们的异常表达导致DNMT3B功能障碍,可能导致GAS7基因甲基化,最终导致其表达减少。然而,补充研究是明确评论的必要条件。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

Predicting the possible effect of miR-203a-3p and miR-29a-3p on <i>DNMT3B</i> and <i>GAS7</i> genes expression.

Predicting the possible effect of miR-203a-3p and miR-29a-3p on <i>DNMT3B</i> and <i>GAS7</i> genes expression.

Predicting the possible effect of miR-203a-3p and miR-29a-3p on <i>DNMT3B</i> and <i>GAS7</i> genes expression.

Predicting the possible effect of miR-203a-3p and miR-29a-3p on DNMT3B and GAS7 genes expression.

Aberrant expression of genes involved in methylation, including DNA methyltransferase 3 Beta (DNMT3B), can cause hypermethylation of various tumor suppressor genes. In this regard, various molecular factors such as microRNAs can play a critical role in regulating these methyltransferase enzymes and eventually downstream genes such as growth arrest specific 7 (GAS7). Accordingly, in the present study we aimed to predict regulatory effect of miRNAs on DNMT3B and GAS7 genes expression in melanoma cell line. hsa-miR-203a-3p and hsa-miR-29a-3p were predicted and selected using bioinformatics software. The Real-time PCR technique was performed to investigate the regulatory effect of these molecules on the DNMT3B and GAS7 genes expression. Expression analysis of DNMT3B gene in A375 cell line showed that there was a significant increase compared to control (p value = 0.0015). Analysis of hsa-miR-203a-3p and hsa-miR-29a-3p indicated the insignificant decreased expression in melanoma cell line compared to control (p value < 0.05). Compared to control, the expression of GAS7 gene in melanoma cells showed a significant decrease (p value = 0.0323). Finally, our findings showed that the decreased expression of hsa-miR-203a-3p and hsa-miR-29a-3p can hypothesize that their aberrant expression caused DNMT3B dysfunction, possible methylation of the GAS7 gene, and ultimately decreased its expression. However, complementary studies are necessary to definite comment.

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
Journal of Integrative Bioinformatics
Journal of Integrative Bioinformatics Medicine-Medicine (all)
CiteScore
3.10
自引率
5.30%
发文量
27
审稿时长
12 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