Small nucleolar RNA host gene 1 (SNHG1) has been identified to function as an oncogene in a large number of human cancers. Nevertheless, the biologic role and underlying molecular mechanism… Click to show full abstract
Small nucleolar RNA host gene 1 (SNHG1) has been identified to function as an oncogene in a large number of human cancers. Nevertheless, the biologic role and underlying molecular mechanism of SNHG1 on cisplatin (DDP)-resistance of NSCLC still unknown. qRT-PCR assay was performed to assess the expression levels of SNHG1 and miR-140-5p. Western blot analysis was used to determine Wnt1, cyclinD1, c-Myc and β-catenin levels. The direct correlation between SNHG1 and miR-140-5p was verified by dual-luciferase reporter assay and RNA immunoprecipitation (RIP) assay. CCK-8 assay and Transwell assay were applied to determine cell proliferation ability, and cell migration and invasion capacities, respectively. Tumor xenograft was performed to confirm the effect of SNHG1 on DDP resistance of NSCLC in vivo. Our data showed SNHG1 was upregulated in DDP-resistant NSCLC tissues and cell lines. SNHG1 knockdown suppressed the proliferation, migration, invasion and DDP-resistance in DDP-resistance NSCLC cell lines in vitro and inhibited tumor growth in vivo. Moreover, SNHG1 repressed miR-140-5p expression by directly binding to miR-140-5p. SNHG1-knockdown-mediated regulatory effect was antagonized by miR-140-5p. Furthermore, Wnt1/β-catenin signaling was involved in SNHG1/miR-140-5p-mediated regulation in DDP-resistance NSCLC cell lines. The results suggested that SNHG1 knockdown ameliorated DDP resistance of NSCLC by sponging miR-140-5p and regulating miR-140-5p/Wnt1/β-catenin pathway, providing a new potential therapeutic target for DDP-resistance NSCLC treatment.
               
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