• MASOUD SOLEIMANI

      Articles written in Journal of Biosciences

    • Overexpression of hsa-miR-939 follows by NGFR down-regulation and apoptosis reduction

      FAHIMEH HOSSEINI AGHDAEI BAHRAM M SOLTANI SADAT DOKANEHIIFARD SEYED JAVAD MOWLA MASOUD SOLEIMANI

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      Neurotrophin receptors play a crucial role in neuronal survival, differentiation and regeneration. Nerve growthfactor receptor (NGFR) or P75NTR is a neurotrophin receptor that is involved in many pathological conditionsincluding cancers. Genetic factors that are involved in regulation of neurotrophin receptors are under intenseinvestigation. MiRNAs are novel regulators of signalling pathways that are candidates for regulation ofneurotrophin receptors. Computational programs predicted that NGFR gene is a bona fide target for hsa-miR-939. RT-qPCR, Western analysis and dual luciferase assay evidences indicated that NGFR transcript is targetedby hsa-miR-939. Also, hsa-miR-939 overexpression brought about down-regulation of NGFR expression in U87cell line, followed by cell death rate reduction, detected by flow cytometry. Taken together, here for the first time,hsa-miR-939 is introduced as a novel key regulator of NGFR expression and its involvement in cell death/survivalprocesses is suggested.

    • Induction of morphological and functional differentiation of human neuroblastoma cells by miR-124

      SAMANEH SHARIF MOHAMMAD HOSSEIN GHAHREMANI MASOUD SOLEIMANI

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      Neuroblastoma is the most common extracranial solid tumour in children, and differentiation is considered its mostappropriate therapy. In this work, we studied effects of miR-124 overexpression on differentiation in M17 cell line as amodel of neuroblastoma cancer. Influence of miR-124 overexpression on differentiation in M17 cells was studied. M17cells were infected with lentivirus that contained miR-124 precursor sequence and followed for 2 weeks to differentiate.Ectopic expression of miR-124 in M17 cells changed the shape of spherical undifferentiated cells to cells with extendedneurites that formed neuronal networks. Overexpression of MiR-124 respectively increased the expression level of markersof beta-Tubulin III, MAP2, SYN, NF-M and Nestin by 16-, 5-, 4-, 2.3- and 2-folds at the messenger RNA level. MiR-124overexpression also increased the protein levels of beta-Tubulin III and MAP2. Moreover, exogenous expression of miR-124significantly increased the intracellular calcium in differentiated M17 cells. Since miR-124 is naturally expressed inneuronal cells and is downregulated in neuroblastoma cancer cells, differentiation with this type of microRNA can be anovel treatment for neuroblastoma cancer.

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