Author/Authors :
Karami, Somayeh Department of Genetics - Faculty of Advanced Science and Technology - Tehran Medical Sciences - Islamic Azad University tehran branch, Tehran, Iran , Kouhkan, Fatemeh Stem Cell Technology Research Center, Tehran, Iran , Rad, Iman Stem Cell Technology Research Center, Tehran, Iran , Tavakolpoor Saleh, Nafiseh Department of Biochemistry - Faculty of Advanced Science and Technology - Tehran Medical Sciences - Islamic Azad University tehran branch, Tehran, Iran , Shokri, Gelareh Stem Cell Technology Research Center, Tehran, Iran , Fallah, Parviz Department of Medical Laboratory Sciences - School of Paramedicine - Alborz University of Medical Sciences, Karaj, Iran , Hashemi, Mehrdad Farhikhtegan Medical Convergence Sciences Research Center - Farhikhtegan Hospital - Tehran University of Medical Sciences - Islamic Azad University tehran branch, 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 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.
Keywords :
Neoplasms , Glioblastoma , MicroRNAs , miR-561 , c-myc