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 interaction with 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 by MTT 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-mesenchymal transition (EMT)-related markers, LIF interleukin 6 family cytokine (LIF), stathmin1 (STMN1), platelet derived growth factor subunit 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 between SNHG1 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 inhibited SNHG1 expression and retarded the viability, proliferation and invasion of GBC cells, accompanied with downregulated N-Cadherin and Vimentin yet upregulated E-Cadherin. MiR-194-5p could competitively bind with SNHG1 and was low-expressed in GBC, revealing the negative correlation between SNHG1 and miR-194-5p. Downregulated miR-194-5p reversed the effects of SNHG1 silencing on viability, proliferation, invasion and EMT-related marker expressions in GBC cells. Additionally, LIF and PDGFA were the target genes of miR-194-5p.

CONCLUSIONS

SNHG1 silencing suppressed the viability, proliferation and invasion of GBC cells via targeting miR-194-5p, revealing a new role of SNHG1 in GBC.