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LncRNA MAGI2-AS3 is downregulated in non-small cell lung cancer and may be a sponge of miR-25

BACKGROUND: This study aimed to investigate the role of lncRNA MAGI2-AS3 in non-small cell lung cancer (NSCLC). METHODS: Expression levels of MAGI2-AS3 and RECK mRNA in two types of tissues (non-tumor and NCSLC) were measured by qPCR. To further investigate the interaction between MAGI2-AS3 and RECK...

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Detalles Bibliográficos
Autores principales: Sui, Yutong, Chi, Wencheng, Feng, Li, Jiang, Jiakang
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7059274/
https://www.ncbi.nlm.nih.gov/pubmed/32138716
http://dx.doi.org/10.1186/s12890-020-1064-7
Descripción
Sumario:BACKGROUND: This study aimed to investigate the role of lncRNA MAGI2-AS3 in non-small cell lung cancer (NSCLC). METHODS: Expression levels of MAGI2-AS3 and RECK mRNA in two types of tissues (non-tumor and NCSLC) were measured by qPCR. To further investigate the interaction between MAGI2-AS3 and RECK, MAGI2-AS3 and RECK expression vectors were transfected into H1993 cells. RESULTS: We found that MAGI2-AS3 and RECK were upregulated and positively correlated in NSCLC. In NSCLC cells, MAGI2-AS3 overexpression led to upregulated RECK. Bioinformatics analysis showed that MAGI2-AS3 may bind miR-25, which can directly target RECK. In NSCLC cells, miR-25 overexpression led to downregulated RECK and attenuated the effects of MAGI2-AS3 overexpression, while MAGI2-AS3 and miR-25 failed to affect each other. Cell invasion and migration analysis showed decreased NSCLC cell invasion and migration rates after MAGI2-AS3 and RECK overexpression. MiR-25 showed opposite role and reduced the effects of MAGI2-AS3 overexpression. CONCLUSION: Therefore, MAGI2-AS3 may sponge miR-25 to upregulate RECK, thereby inhibiting NSCLC cell invasion and migration. TRIAL REGISTRATION: HLJCM20163358592, registered by First Affiliated Hospital, Heilongjiang University of Chinese Medicine at March 3, 2016, prospectively.