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Comprehensive analyses of molecular features, prognostic values, and regulatory functionalities of m(6)A-modified long non-coding RNAs in lung adenocarcinoma

BACKGROUND: Lung adenocarcinoma (LUAD) has a high incidence and recurrence rate. N6-methyladenosine (m(6)A) modification of RNA has become a promising epigenetic marker in tumors. The dysregulation of both RNA m(6)A levels and m(6)A regulator expression levels reportedly affects essential biological...

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Detalles Bibliográficos
Autores principales: Ping, Yili, Huang, Jingjuan, Zhu, Jichao, Sun, Zujun, Shang, Anquan, Chen, Chen, Liu, Wenfang, Li, Dong
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10082542/
https://www.ncbi.nlm.nih.gov/pubmed/37029420
http://dx.doi.org/10.1186/s13148-023-01475-z
Descripción
Sumario:BACKGROUND: Lung adenocarcinoma (LUAD) has a high incidence and recurrence rate. N6-methyladenosine (m(6)A) modification of RNA has become a promising epigenetic marker in tumors. The dysregulation of both RNA m(6)A levels and m(6)A regulator expression levels reportedly affects essential biological processes in various tumors. Long non-coding RNAs (lncRNAs), a subgroup of RNAs over 200 nucleotides in length that do not code for protein, can be modified and regulated by m(6)A, but the relevant profile in LUAD remains unclear. RESULTS: The m(6)A levels of total RNA were decreased in LUAD tumor tissues and cells. Multiple m(6)A regulators were abnormally expressed at both the RNA and protein levels, and were related in expression patterns and functionally synergistic. Our microarray revealed 2846 m(6)A-modified lncRNA transcripts as well as its molecular features, 143 of which were differentially m(6)A-modified and manifested a negative correlation between expression levels and m(6)A modification levels. More than half of the differentially m(6)A-modified lncRNAs associated with dysregulated expression. The 6-MRlncRNA risk signature was a reliable indicator for assessing survival time of LUAD patients. The competitive endogenous regulatory network suggested a potential m(6)A-induced pathogenicity in LUAD. CONCLUSIONS: These data have demonstrated that differential RNA m(6)A modification and m(6)A regulator expression levels were identified in LUAD patients. In addition, this study provides evidence increasing the understanding of molecular features, prognostic values, and regulatory functionalities of m(6)A-modified lncRNAs in LUAD. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1186/s13148-023-01475-z.