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The MiR-561 Suppresses Glioblastoma Cell Proliferation through C-myc Regulation | ||
| Middle East Journal of Cancer | ||
| مقالات آماده انتشار، پذیرفته شده، انتشار آنلاین از تاریخ 02 اسفند 1399 اصل مقاله (1.21 MB) | ||
| نوع مقاله: Original Article | ||
| شناسه دیجیتال (DOI): 10.30476/mejc.2021.83476.1170 | ||
| نویسندگان | ||
Somayeh Karami 1؛ Fatemeh Kouhkan2؛ Iman Rad2؛ Nafiseh Tavakolpoor Saleh3؛ Gelareh Shokri2؛ Parviz Fallah4؛ Mehrdad Hashemi  1
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| 1Department of Genetics, Faculty of Advanced Science and Technology, Tehran Medical Sciences, Islamic Azad University, Tehran, Iran | ||
| 2Stem Cell Technology Research Center, Tehran, Iran | ||
| 3Department of Biochemistry, Faculty of Advanced Science and Technology, Tehran Islamic Azad University of Medical Sciences, Tehran, Iran | ||
| 4Department of Medical Laboratory Sciences, School of Paramedicine, Alborz University of Medical Sciences, Karaj, Iran | ||
| چکیده | ||
| Background: Glioblastoma multiforme (GBM) is the most common primary malignat brain tumor in adults. The modulation of miRNA expression is taken into consideration both as controlling groundwork for cancer development and invasion and as a potential application in GBM-targeted therapies either perse or combined with chemo or radiotherapy. The c-myc overexpression is tightly correlated with GBM progressing growth and malignancy. There is ample evidence showing that microRNAs (miRNAs) are linked to the pathogenesis of several malignancies. However, little is known about the potential role of miRNAs in GBM development. We conducted the present study to find out whether the miR-561 inhibits GBM cells proliferation and survival via controlling the expression of c-myc. Method: In this in vitro study, the U87 cell line was used as a template for lentiviral vector “pCDH-miR-561” construction. HEK293 cell line was transfected with pCDH-miR-561 and its viability (MTT assay) and apoptosis rates (flow cytometry) were monitored. c-myc expression was monitored employing q-RT PCR. In order to search for possible miR-561p targets, we utilized bioinformatics tools of TargetScan and DAVID. Results: Our results confirmed that the overexpression of the miR-561 inhibits cell proliferation and promotes cell apoptosis in GBM cancer cells, which is tightly correlated with the downregulation of c-myc. Conclusion: These findings proposed that the miR-561 has promising qualifications to suppress U87 growth and proliferation via tuning the c-myc, which then makes it a useful model for GBM treatment. | ||
| کلیدواژه‌ها | ||
| Cancer؛ GBM؛ miRNA؛ miR-561؛ c-myc | ||
| اصل مقاله | ||
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This article has been accepted for publication and undergone full peer review but has not been through the copyediting, typesetting, pagination, and proofreading process, which may lead to differences between this version and the Version of Record. Please cite this article as doi: 10.30476/mejc.2021.83476.1170 | ||
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