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MINCR: A long non-coding RNA shared between cancer and neurodegeneration
Affiliation:1. Genomic and post-Genomic Unit, IRCCS Mondino Foundation, Pavia 27100, Italy;2. Department of Biology and Biotechnology "L. Spallanzani", University of Pavia, Pavia 27100, Italy;3. Department of Biomedical and Clinical Sciences "L. Sacco", University of Milan, Milan 20157, Italy;4. Pediatric Clinical Research Center Fondazione "Romeo ed Enrica Invernizzi", University of Milano, Milano 20157, Italy;5. enGenome srl, Pavia 27100, Italy;6. Dipartimento di Scienze Farmacologiche e Biomolecolari (DiSFeB), Centro di Eccellenza sulle Malattie Neurodegenerative, Università degli Studi di Milano, Milano 20157, Italy;7. Neuroncology Unit, IRCCS Mondino Foundation, Pavia 27100, Italy;8. Laboratory of Neurobiology and Neurogenetic, Golgi Cenci Foundation, Abbiategrasso, Milan 20081, Italy;9. Neurology and Neuropathololgy Department Golgi-Cenci Foundation & ASP Golgi-Redaelli, Abbiategrasso, Milan 20081, Italy
Abstract:The multitasking nature of lncRNAs allows them to play a central role in both physiological and pathological conditions. Often the same lncRNA can participate in different diseases. Specifically, the MYC-induced Long non-Coding RNA MINCR is upregulated in various cancer types, while downregulated in Amyotrophic Lateral Sclerosis patients. Therefore, this work aims to investigate MINCR potential mechanisms of action and its implications in cancer and neurodegeneration in relation to its expression levels in SH-SY5Y cells through RNA-sequencing approach. Our results show that MINCR overexpression causes massive alterations in cancer-related genes, leading to disruption in many fundamental processes, such as cell cycle and growth factor signaling. On the contrary, MINCR downregulation influences a small number of genes involved in different neurodegenerative disorders, mostly concerning RNA metabolism and inflammation. Thus, understanding the cause and functional consequences of MINCR deregulation gives important insights on potential pathogenetic mechanisms both in cancer and in neurodegeneration.
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