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Connection Between Mir-490 and Ccnd1 and Gsk3β Genes Play an Effective Role in Wnt Signaling Pathway in Colorectal Cancer Publisher Pubmed



Banoei M1 ; Moghadam NB1 ; Gowdini E1 ; Heidarizadi A1 ; Amanpour S2 ; Abgarmi ZM3 ; Pornour M4 ; Negrini M5 ; Ganji SM1
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Authors Affiliations
  1. 1. Department of Molecular Medicine, Medical Biotechnology Institute, National Institute of Genetic Engineering and Biotechnology, Tehran, Iran
  2. 2. Cancer biology research center, Cancer institute, Tehran University of Medical Sciences, Tehran, Iran
  3. 3. Department of Clinical Biochemistry, School of Medicine, Iranshahr University of Medical Sciences, Iranshahr, Iran
  4. 4. Medical Laser Research Center, Academic Center for Education, Culture and Research (ACECR), Tehran, Iran
  5. 5. Department of Experimental Medicine and Diagnostics, University of Ferrara, Ferrara, Italy

Source: Cell Biochemistry and Biophysics Published:2024


Abstract

The Wnt signaling pathway is identified as one of the main disrupted pathways in Colorectal cancer (CRC). Results from studies focusing on this route will aid greatly in the detection and treatment of CRC. MicroRNAs (MiRs), particularly MiR-490, has emerged as key regulator of gene expression in biological pathways, making it an attractive research target. This is notably true for the Wnt signaling pathway, which is usually disordered in CRC tissues. This study aimed to evaluate the expression level of MiR-490 isomiRs and determine some of its key target genes involved in Wnt signaling pathway in CRC tissues and cell lines, based on experimental and bioinformatics analysis. Elevated expression of GSK3β and CCND1 indicate that the progression of CRC tumor is associated with the inhibitory effect of MiR-490 isomiRs on the Wnt/β-catenin signaling pathway. This finding was supported by the observation of a positive connection between the expression pattern of miR-490-3p and 5p, and CCND1 and GSK3β in CRC. The valuable results of this study provide a means of identifying biomarkers with the potential to either inhibit or activate CRC cellular pathways. © The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature 2024.
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