Simple Summary: The interest in the biological role and clinical impact of long non-coding RNAs (lncRNAs) in multiple myeloma (MM) is continuously expanding. Many studies, mainly involving solid tumors, have strongly suggested the MIAT oncogenic role; more recently, it has been suggested that MIAT may have a role in inducing Bortezomib resistance in MM. However, data concerning MIAT deregulation inMMare virtually absent. In this context, we investigated the expression pattern and the clinical relevance of the lncRNA MIAT in MM, taking advantage of the publicly available CoMMpass database. Our findings prompt further studies to elucidate better the significance of MIAT in MM.The biological impact of long non-coding RNAs (lncRNAs) in multiple myeloma (MM) is becoming an essential aspect of the investigation, which may contribute to understanding the disease's complex pathobiology, providing novel potential therapeutic targets. Herein, we investigated the expression pattern and the clinical relevance of the lncRNA MIAT in MM, taking advantage of the publicly available CoMMpass database. MIAT expression in MM is highly heterogeneous and significantly associated with specific molecular lesions frequently occurring in MM. Transcriptome analyses of MM PCs from patients included in the CoMMpass database indicated a potential involvement of MIAT in different signaling pathways and ribosome biogenesis and assembly. These findings suggest that MIAT deregulation may play a pathogenetic role in MM by affecting both proliferation pathways and, indirectly, the translational process. Although MIAT expression levels seem not to be significantly associated with clinical outcome in multivariate analyses, high MIAT expression levels are associated with bortezomib resistance, this suggesting that MIAT targeting could overcome drug resistance in MM. These findings strongly prompt for further studies investigating the significance of MIAT in MM.

Dissecting the Biological Relevance and Clinical Impact of lncRNA MIAT in Multiple Myeloma

Amodio, Nicola;Gentile, Massimo;Morabito, Fortunato;
2021-01-01

Abstract

Simple Summary: The interest in the biological role and clinical impact of long non-coding RNAs (lncRNAs) in multiple myeloma (MM) is continuously expanding. Many studies, mainly involving solid tumors, have strongly suggested the MIAT oncogenic role; more recently, it has been suggested that MIAT may have a role in inducing Bortezomib resistance in MM. However, data concerning MIAT deregulation inMMare virtually absent. In this context, we investigated the expression pattern and the clinical relevance of the lncRNA MIAT in MM, taking advantage of the publicly available CoMMpass database. Our findings prompt further studies to elucidate better the significance of MIAT in MM.The biological impact of long non-coding RNAs (lncRNAs) in multiple myeloma (MM) is becoming an essential aspect of the investigation, which may contribute to understanding the disease's complex pathobiology, providing novel potential therapeutic targets. Herein, we investigated the expression pattern and the clinical relevance of the lncRNA MIAT in MM, taking advantage of the publicly available CoMMpass database. MIAT expression in MM is highly heterogeneous and significantly associated with specific molecular lesions frequently occurring in MM. Transcriptome analyses of MM PCs from patients included in the CoMMpass database indicated a potential involvement of MIAT in different signaling pathways and ribosome biogenesis and assembly. These findings suggest that MIAT deregulation may play a pathogenetic role in MM by affecting both proliferation pathways and, indirectly, the translational process. Although MIAT expression levels seem not to be significantly associated with clinical outcome in multivariate analyses, high MIAT expression levels are associated with bortezomib resistance, this suggesting that MIAT targeting could overcome drug resistance in MM. These findings strongly prompt for further studies investigating the significance of MIAT in MM.
2021
MIAT
bortezomib
multiple myeloma
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/20.500.11770/342865
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