MicroRNA copy number alterations in the malignant transformation of pleomorphic adenoma to carcinoma ex pleomorphic adenoma

Objective This study used array comparative genomic hybridization to assess copy number alterations (CNAs) involving miRNA genes in pleomorphic adenoma (PA), recurrent pleomorphic adenoma (RPA), residual PA, and carcinoma ex pleomorphic adenoma (CXPA). Materials and Methods We analyzed 13 PA, 4 RPA,...

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Veröffentlicht in:Head & neck 2024-05, Vol.46 (5), p.985-1000
Hauptverfasser: Kimura, Talita de Carvalho, Scarini, João Figueira, Lavareze, Luccas, Kowalski, Luiz Paulo, Coutinho‐Camillo, Cláudia Malheiros, Krepischi, Ana Cristina Victorino, Egal, Erika Said Abu, Altemani, Albina, Mariano, Fernanda Viviane
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Sprache:eng
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Zusammenfassung:Objective This study used array comparative genomic hybridization to assess copy number alterations (CNAs) involving miRNA genes in pleomorphic adenoma (PA), recurrent pleomorphic adenoma (RPA), residual PA, and carcinoma ex pleomorphic adenoma (CXPA). Materials and Methods We analyzed 13 PA, 4 RPA, 29 CXPA, and 14 residual PA using Nexus Copy Number Discovery software. The miRNAs genes affected by CNAs were evaluated based on their expression patterns and subjected to pathway enrichment analysis. Results Across the groups, we found 216 CNAs affecting 2261 miRNA genes, with 117 in PA, 59 in RPA, 846 in residual PA, and 2555 in CXPA. The chromosome 8 showed higher involvement in altered miRNAs in PAs and CXPA patients. Six miRNA genes were shared among all groups. Additionally, miR‐21, miR‐455‐3p, miR‐140, miR‐320a, miR‐383, miR‐598, and miR‐486 were prominent CNAs found and is implicated in carcinogenesis of several malignant tumors. These miRNAs regulate critical signaling pathways such as aerobic glycolysis, fatty acid biosynthesis, and cancer‐related pathways. Conclusion This study was the first to explore CNAs in miRNA‐encoding genes in the PA‐CXPA sequence. The findings suggest the involvement of numerous miRNA genes in CXPA development and progression by regulating oncogenic signaling pathways.
ISSN:1043-3074
1097-0347
1097-0347
DOI:10.1002/hed.27717