Background
This study aimed to investigate the role of lncRNA MAGI2-AS3 in non-small cell lung cancer (NSCLC).
Conclusion
Therefore, MAGI2-AS3 may sponge miR-25 to upregulate RECK, thereby inhibiting NSCLC cell invasion and migration.
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.
Trial registration
HLJCM20163358592, registered by First Affiliated Hospital, Heilongjiang University of Chinese Medicine at March 3, 2016, prospectively.