Up-Regulation of Hsa-miR-11181 in Glioblastoma Multiforme as A Regulator of AKT and TGFBR1 Signalling

(Pages: 421-428)
Hamed Dabiri, M.Sc, 1,#Bahram Mohammad Soltani, Ph.D, 1,*Sadat Dokanehiifard, Ph.D, 1,#Amin Jahanbakhshi, Ph.D, 2Mehdi Khaleghi, Ph.D, 3
Molecular Genetics Department, Faculty of Biological Sciences, Tarbiat Modares University, Tehran, Iran
Stem Cell and Regenerative Medicine Research Centre, Iran University of Medical Sciences (IUMS), Tehran, Iran
Department of Neurosurgery, Shariati Hospital, Tehran University of Medical Science (TUMS), Tehran, Iran
Molecular Genetics Department, Faculty of Biological Sciences, Tarbiat Modares University, Tehran, Iran
Stem Cell and Regenerative Medicine Research Centre, Iran University of Medical Sciences (IUMS), Tehran, Iran
Department of Neurosurgery, Shariati Hospital, Tehran University of Medical Science (TUMS), Tehran, Iran
*Corresponding Address: P.O.Box: 14155-111 Molecular Genetics Department Faculty of Biological Sciences Tarbiat Modares University Tehran Iran Email:soltanib@modares.ac.ir

These authors contributed equally to this work.

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Dabiri Hamed, Mohammad Soltani Bahram, Dokanehiifard Sadat, Jahanbakhshi Amin, Khaleghi Mehdi. Up-Regulation of Hsa-miR-11181 in Glioblastoma Multiforme as A Regulator of AKT and TGFBR1 Signalling . Cell J. 2021; 23(4): 421-428.

Abstract

Objective

MicroRNAs (miRNAs) are short non-coding RNAs that play a role in post-transcriptional regulation of gene expression. Hsa-miR-11181 was originally introduced as a regulator of genes involved in some brain tumours. Due to the high expression of Hsa-miR-11181 in limited glioblastoma brain tumours, in this study we intend to assess the expressions of Hsa-miR-11181 and Has-miR11181-3p in brain tumour tissues and attribute new target genes to these miRNAs.

Materials and Methods

In this experimental study, total RNA from brain tissue samples was extracted for real-time quantitative polymerase chain reaction (RT-qPCR) analysis after cDNA synthesis. In order to confirm a direct interaction of Hsa-miR-11181 with two target genes, the 3ˊ UTR of AKT2 and transforming growth factor-beta receptor 1 (TGFBR1) were cloned separately for assessment by the dual luciferase assay.

Results

RT-qPCR analysis indicated that both Hsa-miR-11181-5p and Hsa-miR-11181-3p specifically up-regulated in higher grades of glioma tumours versus other brain tumour types. Consistently, lower expression levels of AKT2 and TGFBR1 were detected in higher grade gliomas compared to other types of brain tumours, which was inverse to the level of expression detected for the heparin-binding EGF-like growth factor (HBEGF) gene. The results of the dual luciferase assay supported a direct interaction of Hsa-miR-11181 with the 3ˊ UTR sequences of the AKT2 and TGFBR1 genes.

Conclusion

Overall, our data suggest that miR-1118 is a potential molecular biomarker for discrimination of glioma brain tumours from other brain tumour types.