Background: Non-small cell lung cancer (NSCLC) is the most common type of lung carcinoma. Long non-coding RNA (lncRNA) small nucleolar RNA host gene 14 (SNHG14 ) was identified to participate in tumor progression. However, the mechanism and functions of SNHG14  were rarely reported in NSCLC progression.
Methods: The relative gene expression was tested by qRT-PCR. Cell viability, apoptosis, migration and invasion were measured by MTT assay, flow cytometry, and transwell migration and invasion assays, respectively. The interactions between miR-382-5p  and SNHG14  or SPIN1  were predicted by starBase and confirmed by the dual-luciferase reporter assay and RNA pull-down assay. The protein level of SPIN1  was evaluated by Western blot assay.
Results: The levels of SNHG14  and SPIN1  were significantly increased, while the level of miR-382-5p  was apparently reduced in NSCLC tissues and cells. SNHG14  was verified to sponge miR-382-5p  and SPIN1  was identified as a direct target of miR-382-5p . SNHG14  depletion repressed cell viability, migration and invasion, but induced the apoptotic rate by targeting miR-382-5p . miR-382-5p  overexpression blocked cell viability, metastasis and promoted cell apoptosis by regulating SPIN1 . SNHG14  silencing down-regulated SPIN1  expression by sponging miR-382-5p .
Conclusion: SNHG14  facilitated NSCLC progression by regulating SPIN1  expression via targeting miR-382-5p .
Keywords: lncRNA SNHG14 , miR-382-5p , SPIN1 , tumor progression, NSCLC