Silencing SNHG1 Suppresses Viability, Proliferation and Invasion of Gallbladder Carcinoma Cells via Targeting miR-194-5p

Objective Long non-coding RNA small nuclear host gene 1 (LncRNA SNHG1) was implicated in several malignancies, but its role and interactionwith microRNAs (miRs) in gallbladder cancer (GBC) were awaited to be addressed. Methods Clinical GBC tissues were collected. After transfection, GBC cell viability, proliferation and invasion were determined byMTT assay, colony formation assay and Transwell assay, respectively. Target gene and potential binding sites were predicted,followed by confirmation with dual-luciferase reporter assay. Relative expressions of SNHG1, miR-194-5p, epithelial-mesenchymaltransition (EMT)-related markers, LIF interleukin 6 family cytokine (LIF), stathmin1 (STMN1), platelet derived growth factorsubunit A (PDGFA), insulin like growth factor 1 receptor (IGF1R) and signal transducer and activator of transcription 1 (STAT1)were quantified by quantitative real-time polymerase chain reaction (qRT-PCR) and western blot as needed. Correlation betweenSNHG1 and miR-194-5p in GBC was analyzed. Results High expression of SNHG1 was observed in both GBC tissues and cells, and it was associated with tumor sizes. ShSNHG1 inhibitedSNHG1 expression and retarded the viability, proliferation and invasion of GBC cells, accompanied with downregulated N-Cadherinand Vimentin yet upregulated E-Cadherin. MiR-194-5p could competitively bind with SNHG1 and was low-expressed in GBC, revealingthe negative correlation between SNHG1 and miR-194-5p. Downregulated miR-194-5p reversed the effects of SNHG1 silencing onviability, proliferation, invasion and EMT-related marker expressions in GBC cells. Additionally, LIF and PDGFA were the targetgenes of miR-194-5p. Conclusions SNHG1 silencing suppressed the viability, proliferation and invasion of GBC cells via targeting miR-194-5p, revealing a newrole of SNHG1 in GBC.