Somayeh Karami - Department of Genetics, Faculty of Advanced Science and Technology, Tehran Medical Sciences, Islamic Azad University, Tehran, Iran
Fatemeh Kouhkan - Stem Cell Technology Research Center, Tehran, Iran
Iman Rad - Stem Cell Technology Research Center, Tehran, Iran
Nafiseh Tavakolpoor Saleh - Department of Biochemistry, Faculty of Advanced Science and Technology, Tehran Medical Sciences, Islamic Azad University, Tehran, Iran
Gelareh Shokri - Stem Cell Technology Research Center, Tehran, Iran
Parviz Fallah - Department of Medical Laboratory Sciences, School of Paramedicine, Alborz University of Medical Sciences, Karaj, Iran
Mehrdad Hashemi - Farhikhtegan Medical Convergence Science Research Center, Farhikhtegan Hospital, Tehran University of Medical Sciences, Islamic Azad University, Tehran, Iran

Background: Glioblastoma multiforme (GBM) is the most common primary malignat brain tumor in adults. The modulation of miRNA expression is considered 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-۵۶۱ inhibits GBM cells proliferation and survival via controlling the expression of c-myc. Method: In this in vitro study, the U۸۷ cell line was used as a template for lentiviral vector “pCDH-miR-۵۶۱” construction. HEK۲۹۳ cell line was transfected with pCDHmiR- ۵۶۱ 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-۵۶۱p targets, we utilized bioinformatics tools of TargetScan and DAVID. Results: Our results confirmed that the overexpression of the miR-۵۶۱ 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-۵۶۱ has promising qualifications to suppress U۸۷ growth and proliferation via tuning the c-myc, which then makes it a useful model for GBM treatment.

Neoplasms, Glioblastoma, MicroRNAs, miR-۵۶۱, c-myc