Bozgeyik, Esra2022-05-112022-05-1120202214-5400https://doi.org/10.1016/j.mgene.2019.100614https://hdl.handle.net/20.500.11776/4919Although there are several studies, biological function and therapeutic potential of miR-17-5p in breast cancer carcinogenesis remains muchly elusive. Specifically, its interaction with several cancer-associated genes remains unexplored in breast cancer. Here, we aimed to demonstrate the biological function and therapeutic potential of miR-17-5p in breast cancer through determination of the interactions between cancer-associated genes and miR-17-5p. MFC-7 breast cancer cells used in the study and cells were transfected with miR-17-5p miRNA mimics to ectopically overexpress miR-17-5p. MiR-17-5p expression levels and expression changes of cancer-associated genes were determined by using qPCR method. Expression levels of miR-17-5p were significantly enhanced following 72 h of mimic transfections as compared to scrambled control and blank control. Overexpression of miR-17-5p led to differential expression of several cancer-associated genes. Notably, BECN, CDKN2B and AIFM genes were significantly altered. Although not significant, expression levels of BAX, BCLXL, VIM, BCL2, MTOR, RB1, AKT1, XIAP, P53, and PTEN genes were found to be slightly elevated whereas expression levels of BCL-2, VIM and AKT1 were found to be decreased. Results of the present study indicate that miR-17-5p can act as both tumor suppressor and tumor promoter oncomiR in breast cancer. © 2019 Elsevier B.V.en10.1016/j.mgene.2019.100614info:eu-repo/semantics/closedAccessAIFMBECNBreast cancerCDKN2BmiR-17-5pmiRNAapoptosis inducing factorbeclin 1cyclin dependent kinase inhibitor 2Bmammalian target of rapamycinmicroRNAmicrorna 17 5pphosphatidylinositol 3,4,5 trisphosphate 3 phosphataseprotein Baxprotein bcl 2protein bcl xlprotein kinase Bprotein p53unclassified drugvimentinX linked inhibitor of apoptosisArticlebreast cancer cell linecancer growthcarcinogenesiscell culturecell proliferationcontrolled studyDNA synthesisdown regulationgene controlgene expressiongene interactiongene overexpressiongene targetinggenetic transfectionhumanhuman cellmRNA expression assaypriority journalprotein expressionquantitative analysisreal time polymerase chain reactionregulatory mechanismreverse transcription polymerase chain reactionRNA extractionRNA isolationsignal transductiontumor suppressor geneupregulationWestern blottingArticle24N/AWOS:0005257507000432-s2.0-85073827804Q4