Napolitano, Antonella (2025) Understanding the role of the long non-coding RNA Rhabdomyosarcoma 2-Associated Transcript in glioblastoma. [Tesi di dottorato]
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| Tipologia del documento: | Tesi di dottorato |
|---|---|
| Lingua: | English |
| Titolo: | Understanding the role of the long non-coding RNA Rhabdomyosarcoma 2-Associated Transcript in glioblastoma |
| Autori: | Autore Email Napolitano, Antonella antonella.napolitano@unina.it |
| Data: | 11 Dicembre 2025 |
| Numero di pagine: | 83 |
| Istituzione: | Università degli Studi di Napoli Federico II |
| Dipartimento: | Medicina Molecolare e Biotecnologie Mediche |
| Dottorato: | Medicina molecolare e biotecnologie mediche |
| Ciclo di dottorato: | 38 |
| Coordinatore del Corso di dottorato: | nome email Santoro, Massimo massimo.santoro@unina.it |
| Tutor: | nome email Santoro, Massimo [non definito] De Martino, Marco [non definito] |
| Data: | 11 Dicembre 2025 |
| Numero di pagine: | 83 |
| Parole chiave: | Glioblastoma; long non-coding RNA; tumor-suppressor |
| Settori scientifico-disciplinari del MIUR: | Area 06 - Scienze mediche > MED/04 - Patologia generale |
| Informazioni aggiuntive: | ciclo 38 |
| Depositato il: | 22 Dic 2025 10:11 |
| Ultima modifica: | 12 Ago 2026 05:37 |
| URI: | https://www.fedoa.unina.it/id/eprint/16043 |
Abstract
Glioblastoma (GBM) is the most aggressive primary brain tumor in adults, characterized by rapid proliferation, extensive invasion, and resistance to standard therapies. Long non-coding RNAs (lncRNAs) have emerged as critical regulators of cancer progression, yet the functions of many remain poorly understood. This study investigates the role of the brain-enriched lncRNA Rhabdomyosarcoma 2-Associated Transcript (RMST) in GBM pathogenesis. Transcriptomic analyses and qPCR validation revealed a marked downregulation of RMST across various histological types of brain tumours, from oligodendroglioma to GBM, parallel to increasing tumour grade. RMST overexpression correlated positively with patient overall survival, supporting its potential as a prognostic biomarker. Functional assays demonstrated that RMST overexpression significantly inhibited GBM cell proliferation, clonogenicity, migration, and invasion, while enhancing sensitivity to the chemotherapeutic agent temozolomide (TMZ). RMST overexpression also suppressed the expression of key Extra Cellular Matrix (ECM) and epithelial-to-mesenchymal transition (EMT)-associated genes, including SNAIL, SLUG and N-cadherin, while upregulating E-cadherin, suggesting a reversal of the mesenchymal phenotype. Interestingly, RNA-seq analysis revealed that RMST overexpression is also associated with alterations in metabolic gene expression, indicating that this lncRNA may contribute to metabolic reprogramming in GBM cells. These findings support a model whereby RMST functions as a tumor suppressor lncRNA in GBM by attenuating malignant phenotype and enhancing therapy responsiveness. Although further mechanistic and in vivo studies are needed, these data indicate that RMST represents a promising candidate for biomarker development and therapeutic targeting in high-grade gliomas.
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