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JCR 2016
جستجوی مقالات
پنجشنبه 27 آذر 1404
Cell Journal
، جلد ۲۲، شماره ۲، صفحات ۱۵۸-۱۶۴
عنوان فارسی
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کلیدواژههای فارسی مقاله
عنوان انگلیسی
Hsa-miR-587 Regulates TGFβ/SMAD Signaling and Promotes Cell Cycle Progression
چکیده انگلیسی مقاله
Objective
Transforming growth factor beta/single mothers against decapentaplegic (TGFβ/SMAD) signaling pathway plays important roles in various biological processes. It acts as a tumor suppressor during the early stages of cancer progression. Discovering the regulators of this pathway provides important options for therapeutic strategies. Here, we searched for candidate microRNAs (miRNAs) that potentially target the critical components of the TGFβ signaling pathway.
Materials and Methods
In the current experimental study, we first predicted miRNAs that target TGFβ components using a bioinformatics software. After that, quantitative real-time polymerase chain reaction (RT-qPCR) was used to detect the expression of miR-587, TGFBR2, SMAD4, p21, CCND1 and c-MYC genes in transfected HEK293T and HCT116 cells. Dual Luciferase assay was performed to analyze the interactions between miRNAs and the target genes. Propidium iodide flow cytometry was used to determine cell cycle progression in HEK293T and HCT116 cells under hsa-miR-587 (miR-587) overexpression circumstances.
Results
Multiple miRNA responsive elements (MREs) were predicted for miR-587 within the 3’UTRs of the TGFBR2 and SMAD4 genes. Overexpression of miR-587 in HEK293T and HCT116 cells resulted in downregulation of TGFBR2 and SMAD4 genes. In addition, a downstream target gene of TGFβ/SMAD signaling, P21, was significantly downregulated in the HCT116 cells overexpressing miR-587. Dual luciferase assay analysis provided evidence that there is a direct interaction between miR-587 and the 3’UTR sequences of TGFBR2 and SMAD4 genes. Moreover, miR-587 overexpression in HEK293T and HCT116 cells resulted in reducing the SubG1 cell populations in both cell lines, as detected by flow cytometry.
Conclusion
Altogether, our data revealed an important role for miR-587 in regulating TGFβ/SMAD signaling and promoting cell cycle progression. These characteristics suggest that miR-587 is an important candidate for cancer therapy research.
کلیدواژههای انگلیسی مقاله
Cancer, Cell cycle, TGFβ/SMAD Signaling
نویسندگان مقاله
Mahnaz Jahangirimoez |
.Department of Molecular Genetics, Faculty of Biological Sciences, Tarbiat Modares University, Tehran, Iran
Abdallah Medlej |
.Department of Molecular Genetics, Faculty of Biological Sciences, Tarbiat Modares University, Tehran, Iran
Mahmoud Tavallaie |
.Department of Medical Genetics, Baqiyatallah University of Medical Sciences, Tehran, Iran
Bahram Mohammad Soltani |
.Department of Molecular Genetics, Faculty of Biological Sciences, Tarbiat Modares University, Tehran, Iran
نشانی اینترنتی
https://www.celljournal.org/article_250635_2e380ab6021cc0ad33617447d82935db.pdf
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