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The function of lncRNA EMX2OS/miR-653-5p and its regulatory mechanism in lung adenocarcinoma

This study aimed to evaluate the significance of EMX2OS in lung adenocarcinoma (LUAD) prognosis and development and its potential molecular mechanism. Paired tissue samples were collected from 117 LUAD patients. The EMX2OS expression level was detected by PCR and correlated with patients’ clinicopat...

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Detalles Bibliográficos
Autores principales: Ma, Lina, Zhang, Lu, Li, Lin, Zhao, Li
Formato: Online Artículo Texto
Lenguaje:English
Publicado: De Gruyter 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10105521/
https://www.ncbi.nlm.nih.gov/pubmed/37069939
http://dx.doi.org/10.1515/med-2023-0686
Descripción
Sumario:This study aimed to evaluate the significance of EMX2OS in lung adenocarcinoma (LUAD) prognosis and development and its potential molecular mechanism. Paired tissue samples were collected from 117 LUAD patients. The EMX2OS expression level was detected by PCR and correlated with patients’ clinicopathological features by a series of statistical analyses. The function of EMX2OS in cell proliferation and metastasis was evaluated by CCK8 and Transwell assay. In mechanism, the interaction between EMX2OS and miR-653-5p was assessed by the dual-luciferase reporter assay, and the regulatory effect of miR-653-5p on EMX2OS tumor suppressor role was also estimated. Significant downregulation of EMX2OS and its negative correlation with miR-653-5p was observed in LUAD tissues. A significant relationship was revealed in EMX2OS with TNM stage, lymph node metastasis, and differentiation of LUAD patients, and associated with the poor prognosis of patients. EMX2OS suppressed the proliferation and metastasis of LUAD cells and negatively regulated the expression of miR-653-5p. The overexpression of miR-653-5p could reverse the inhibitory effect of EMX2OS on LUAD cells. In conclusion, EMX2OS served as a biomarker in LUAD that indicated patients’ prognosis and regulated cellular processes via regulating miR-653-5p.