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Mir-17-92A-1 Cluster Host Gene: A Key Regulator in Colorectal Cancer Development and Progression Publisher Pubmed



Mohajeri Khorasani A1, 2, 3 ; Mohammadi S1, 2, 3 ; Raghibi A4 ; Haj Mohammad Hassani B1, 2, 3 ; Bazghandi B5 ; Mousavi P2
Authors
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Authors Affiliations
  1. 1. Department of Medical Genetics, Faculty of Medicine, Hormozgan University of Medical Sciences, Bandar Abbas, Iran
  2. 2. Molecular Medicine Research Center, Hormozgan Health Institute, Hormozgan University of Medical Sciences, Bandar Abbas, Iran
  3. 3. Student Research Committee, Hormozgan University of Medical Sciences, Bandar Abbas, Iran
  4. 4. Department of Medical Genetics, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran
  5. 5. Protein Research Center, Shahid Beheshti University, Tehran, Iran

Source: Clinical and Experimental Medicine Published:2024


Abstract

Colorectal cancer (CRC), recognized among the five most prevalent malignancies and most deadly cancers, manifests multifactorial influences stemming from environmental exposures, dietary patterns, age, and genetic predisposition. Although substantial progress has been made in comprehending the etiology of CRC, the precise genetic components driving its pathogenesis remain incompletely elucidated. Within the expansive repertoire of non-coding RNAs, particular focus has centered on the miR-17-92a-1 cluster host gene (MIR17HG) and its associated miRNAs, which actively participate in diverse cellular processes and frequently exhibit heightened expression in various solid tumors, notably CRC. Therefore, the primary objective of this research is to undertake an extensive inquiry into the regulatory mechanisms, structural features, functional attributes, and potential diagnostic and therapeutic implications associated with this cluster in CRC. Furthermore, the intricate interplay between this cluster and the development and progression of CRC will be explored. Our findings underscore the upregulation of the miR-17-92a-1 cluster host gene (MIR17HG) and its associated miRNAs in CRC compared to normal tissues, thus implying their profound involvement in the progression of CRC. Collectively, these molecules are implicated in critical oncogenic processes, encompassing metastatic activity, regulation of apoptotic pathways, cellular proliferation, and drug resistance. Consequently, these findings shed illuminating insights into the potential of MIR17HG and its associated miRNAs as promising targets for therapeutic interventions in the management of CRC. Graphical abstract: (Figure presented.) © The Author(s) 2024.
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