Silencing of SNHG6 induced cell autophagy by targeting miR-26a-5p/ULK1 signaling pathway in human osteosarcoma

BackgroundlncRNAs have been proved to play crucial parts in various human cytopathology and cell physiology, including tumorigenesis. Down-regulated lncRNAs SNHG6 have shown great cell proliferation inhibitory effects in cancer development. Here we investigated how SNHG6 effected human osteosarcoma (OS) development and progression. Methods: Reverse transcription-quantitative PCR was performed to detect SNHG6 mRNA level in both OS tissues and cell lines. MTT and colony formation assays were used to determine the growth impact of SNHG6. Wound healing and trans-well assay were performed to measure the invasion effect of SNHG6. Western blotting were utilized to dissect molecular mechanisms.ResultsWe identified SNHG6 as a lncRNAs that significantly up-regulated in OS tissues and cells, patients with high SNHG6 expression suffered more malignant metastasis and shorter survival times. Furthermore, silencing of SNHG6 in OS significantly inhibited OS cell growth, weakened cell invasion capacity, arrested cell cycle at G0/G1 phase, and induced cell apoptosis. Additionally, mechanism assays suggested that SNHG6 could competitively sponging miR-26a-5p thereby regulating ULK1, and induced cell apoptosis and autophagy by targeting caspase3 and ATF3. Conclusions: Our findings demonstrated that SNHG6 acted as an oncogene in osteosarcoma cells through regulating miR-26a-5p/ULK1 at a post-transcriptional level. SNHG6 might serve as a candidate prognostic biomarker and a target for novel therapies of osteosarcoma patients.