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Article

MIAT Is an Upstream Regulator of NMYC and the Disruption of the MIAT/NMYC Axis Induces Cell Death in NMYC Amplified Neuroblastoma Cell Lines

1
Department of Pediatric Hematology and Oncology, 2nd Faculty of Medicine, Charles University and Motol University Hospital, V Uvalu 84, 150 06 Prague, Czech Republic
2
Department of Pathology and Molecular Medicine, 2nd Faculty of Medicine, Charles University and Motol University Hospital, V Uvalu 84, 150 06 Prague, Czech Republic
*
Author to whom correspondence should be addressed.
Academic Editor: Fabio Morandi
Int. J. Mol. Sci. 2021, 22(7), 3393; https://doi.org/10.3390/ijms22073393
Received: 5 March 2021 / Revised: 22 March 2021 / Accepted: 22 March 2021 / Published: 25 March 2021
(This article belongs to the Special Issue Molecular Determinants of Neuroblastoma)
Neuroblastoma (NBL) is the most common extracranial childhood malignant tumor and represents a major cause of cancer-related deaths in infants. NMYC amplification or overexpression is associated with the malignant behavior of NBL tumors. In the present study, we revealed an association between long non-coding RNA (lncRNA) myocardial infarction associated transcript (MIAT) and NMYC amplification in NBL cell lines and MIAT expression in NBL tissue samples. MIAT silencing induces cell death only in cells with NMYC amplification, but in NBL cells without NMYC amplification it decreases only the proliferation. MIAT downregulation markedly reduces the NMYC expression in NMYC-amplified NBL cell lines and c-Myc expression in NMYC non-amplified NBL cell lines, but the ectopic overexpression or downregulation of NMYC did not affect the expression of MIAT. Moreover, MIAT downregulation results in decreased ornithine decarboxylase 1 (ODC1), a known transcriptional target of MYC oncogenes, and decreases the glycolytic metabolism and respiratory function. These results indicate that MIAT is an upstream regulator of NMYC and that MIAT/NMYC axis disruption induces cell death in NMYC-amplified NBL cell lines. These findings reveal a novel mechanism for the regulation of NMYC in NBL, suggesting that MIAT might be a potential therapeutic target, especially for those with NMYC amplification. View Full-Text
Keywords: neuroblastoma; NMYC amplification; lncRNA MIAT; cell metabolism neuroblastoma; NMYC amplification; lncRNA MIAT; cell metabolism
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MDPI and ACS Style

Feriancikova, B.; Feglarova, T.; Krskova, L.; Eckschlager, T.; Vicha, A.; Hrabeta, J. MIAT Is an Upstream Regulator of NMYC and the Disruption of the MIAT/NMYC Axis Induces Cell Death in NMYC Amplified Neuroblastoma Cell Lines. Int. J. Mol. Sci. 2021, 22, 3393. https://doi.org/10.3390/ijms22073393

AMA Style

Feriancikova B, Feglarova T, Krskova L, Eckschlager T, Vicha A, Hrabeta J. MIAT Is an Upstream Regulator of NMYC and the Disruption of the MIAT/NMYC Axis Induces Cell Death in NMYC Amplified Neuroblastoma Cell Lines. International Journal of Molecular Sciences. 2021; 22(7):3393. https://doi.org/10.3390/ijms22073393

Chicago/Turabian Style

Feriancikova, Barbara, Tereza Feglarova, Lenka Krskova, Tomas Eckschlager, Ales Vicha, and Jan Hrabeta. 2021. "MIAT Is an Upstream Regulator of NMYC and the Disruption of the MIAT/NMYC Axis Induces Cell Death in NMYC Amplified Neuroblastoma Cell Lines" International Journal of Molecular Sciences 22, no. 7: 3393. https://doi.org/10.3390/ijms22073393

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