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.
Conclusion
SNHG14 facilitated NSCLC progression by regulating SPIN1 expression via targeting miR-382-5p.
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.