Background
Lung cancer mainly includes non-small cell lung cancer (NSCLC). Lung adenocarcinoma (LUAD) is the main subtype of NSCLC. Long non-coding RNAs (LncRNAs) had been found to exert numerous functions on the progressions of cancers. MicroRNAs often exist as the target of LncRNAs to regulate a series of signaling pathways in human. We explored the effects and molecular mechanism of LncRNA SGMS1-AS1 on the procedures of LUAD cells.
Conclusion
LncRNA SGMS1-AS1 inhibits the proliferation, invasion, migration and EMT progression of LUAD cells via targeting miR-106a-5p/MYLIP axis.
Methods
The ENCORI and GEPIA databases were used to analyze the differences in SGMS1, miR-106a-5p, and MYLIP between LUAD and normal tissue. Their expression levels were examined by RT-PCR. CCK8, colony formation, migration, and invasion assay were conducted in LUAD cells which had silenced SGMS1-AS1. To verify the relationship between SGMS1-AS1, miR-106a-5p, and MYLIP, we overexpressed miR-106a-5p inhibitor or MYLIP in LUAD cells after decreasing SGMS1-AS1 and repeated the above assays.
Results
SGMS1-AS1 was downregulated in LUAD tissue as well as cells, which was related to good prognosis of patients with lung adenocarcinoma. Additionally, knockdown of SGMS1-AS1 promoted proliferation, migration, invasion, and epithelial mesenchymal transition (EMT) progression of LUAD cells, which meant that SGMS1-AS1 inhibited the progression of LUAD cells. Furthermore, miR-106a-5p was the direct target of SGMS1-AS1 and transfecting miR-106a-5p inhibitor could reversed the impact induced by knockdown of SGMS1-AS1. Subsequently, we found that MYLIP was the target of miR-106a-5p, which was negatively correlated with miR-106a-5p, but had high positive correlation with SGMS1-AS1. Consistently, overexpression MYLIP partly eliminated the effects on A549 cells induced by silencing of SGMS1-AS1.