{"title":"MiR-9 Promotes Apoptosis <i>Via</i> Suppressing SMC1A Expression in GBM Cell Lines.","authors":"Yong Zu, Zhichuan Zhu, Min Lin, Dafeng Xu, Yongjun Liang, Yueqian Wang, Zhengdong Qiao, Ting Cao, Dan Yang, Lili Gao, Pengpeng Jin, Peng Zhang, Jianjun Fu, Jing Zheng","doi":"10.2174/2213988501711010031","DOIUrl":null,"url":null,"abstract":"<p><strong>Objective: </strong>Glioblastomas multiforme (GBM) is the most malignant brain cancer, which presented vast genomic variation with complicated pathologic mechanism.</p><p><strong>Method: </strong>MicroRNA is a delicate post-transcriptional tuner of gene expression in the organisms by targeting and regulating protein coding genes. MiR-9 was reported as a significant biomarker for GBM patient prognosis and a key factor in regulation of GBM cancer stem cells. To explore the effect of miR-9 on GBM cell growth, we over expressed miR-9 in U87 and U251 cells. The cell viability decreased and apoptosis increased after miR-9 overexpression in these cells. To identify the target of miR-9, we scanned miR-9 binding site in the 3'UTRs region of expression SMC1A (structural maintenance of chromosomes 1A) genes and designed a fluorescent reporter assay to measure miR-9 binding to this region. Our results revealed that miR-9 binds to the 3'sUTR region of SMC1A and down-regulated SMC1A expression.</p><p><strong>Result: </strong>Our results indicated that miR-9 was a potential therapeutic target for GBM through triggering apoptosis of cancer cells.</p>","PeriodicalId":10755,"journal":{"name":"Current Chemical Genomics and Translational Medicine","volume":"11 ","pages":"31-40"},"PeriodicalIF":0.0000,"publicationDate":"2017-07-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5564015/pdf/","citationCount":"10","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Current Chemical Genomics and Translational Medicine","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.2174/2213988501711010031","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2017/1/1 0:00:00","PubModel":"eCollection","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 10
Abstract
Objective: Glioblastomas multiforme (GBM) is the most malignant brain cancer, which presented vast genomic variation with complicated pathologic mechanism.
Method: MicroRNA is a delicate post-transcriptional tuner of gene expression in the organisms by targeting and regulating protein coding genes. MiR-9 was reported as a significant biomarker for GBM patient prognosis and a key factor in regulation of GBM cancer stem cells. To explore the effect of miR-9 on GBM cell growth, we over expressed miR-9 in U87 and U251 cells. The cell viability decreased and apoptosis increased after miR-9 overexpression in these cells. To identify the target of miR-9, we scanned miR-9 binding site in the 3'UTRs region of expression SMC1A (structural maintenance of chromosomes 1A) genes and designed a fluorescent reporter assay to measure miR-9 binding to this region. Our results revealed that miR-9 binds to the 3'sUTR region of SMC1A and down-regulated SMC1A expression.
Result: Our results indicated that miR-9 was a potential therapeutic target for GBM through triggering apoptosis of cancer cells.
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