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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.    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.    Conclusion  LncRNA SGMS1‐AS1 inhibits the proliferation, invasion, migration and EMT progression of LUAD cells via targeting miR‐106a‐5p/MYLIP axis.

LncRNA SGMS1‐AS1 regulates lung adenocarcinoma cell proliferation, migration, invasion, and EMT progression via miR‐106a‐5p/MYLI9 axis