SNHG14 silencing suppresses the progression and promotes cisplatin sensitivity in non-small cell lung cancer.

Long non-coding RNAs (lncRNAs) small nucleolar RNA host gene 14 (SNHG14) has been identified as an oncogene involved in the progression of various human cancers. Nevertheless, the functional role and molecular mechanism of SNHG14 on NSCLC remain largely elusive. qRT-PCR assay was performed to detect the levels of SNHG14, miR-34a and high mobility group box 1 (HMGB1) mRNA. HMGB1 protein level was assessed by western blot analysis. CCK-8 assay was used to determine the IC50 value of cisplatin (CDDP), and transwell assays were employed to detect cell migration and invasion abilities. Cell apoptosis was determined by flow cytometric analysis. Dual-luciferase reporter assay, RNA immuoprecipitation assay and RNA pull-down assay were performed to confirm the interaction between SNHG14 and miR-34a, or miR-34a and HMGB1. Our data demonstrated that SNHG14 was upregulated in NSCLC cells, and SNHG14 silencing repressed the migration, invasion while accelerated the apoptosis of NSCLC cells. Moreover, we manifested that SNHG14 silencing promoted NSCLC cell sensitivity to CDDP. SNHG14 repressed miR-34a expression by binding to miR-34a. Additionally, SNHG14 regulated HMGB1 expression by sponging miR-34a. SNHG14 silencing exerted its regulatory effect by miR-34a and HMGB1 mediated the regulatory effect of miR-34a on NSCLC cells. In conclusion, SNHG14 silencing suppressed NSCLC progression at least partly by miR-34a/HMGB1 axis in vitroand promoted NSCLC cell sensitivity to CDDP, highlighting that SNHG14 might be a potential target for NSCLC therapy.