Document Type : Original Article(s)
Authors
- Somayeh Karami 1
- Fatemeh Kouhkan 2
- Iman Rad 2
- Nafiseh Tavakolpoor Saleh 3
- Gelareh Shokri 2
- Parviz Fallah 4
- Mehrdad Hashemi 5, 1
1 Department of Genetics, Faculty of Advanced Science and Technology, Tehran Medical Sciences, Islamic Azad University, Tehran, Iran
2 Stem Cell Technology Research Center, Tehran, Iran
3 Department of Biochemistry, Faculty of Advanced Science and Technology, Tehran Medical Sciences, Islamic Azad University, Tehran, Iran
4 Department of Medical Laboratory Sciences, School of Paramedicine, Alborz University of Medical Sciences, Karaj, Iran
5 Farhikhtegan Medical Convergence Science Research Center, Farhikhtegan Hospital, Tehran University of Medical Sciences, Islamic Azad University, Tehran, Iran
Abstract
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-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 pCDHmiR- 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.
Keywords
How to cite this article:
Karami S, Kouhkan F, Rad I, Tavakolpoor Saleh N, Shokri G, Fallah, P, et al. The miR-561 suppresses glioblastoma cell proliferation through c-myc regulation. Middle East J Cancer. 2021;12(3):321-31. doi: 10.30476/mejc.2021.83476.1170.
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