SNHG10 Promotes Cell Proliferation and Migration in Gastric Cancer by Targeting miR-495-3p/CTNNB1 Axis

Background Long non-coding RNAs have been acknowledged as the crucial regulators in the progression of human cancers, including gastric cancer (GC). Small nucleolar RNA host gene 10 (SNHG10) has been identified as an oncogene in several cancer types. Nonetheless, it is unclear whether SNHG10 exerts functions in GC cells. Aims The aims of the current study were to explore the function and underlying mechanism of SNHG10 in GC. Methods The expression levels of SNHG10, miR-495-3p and catenin beta 1 (CTNNB1) were detected by RT-qPCR. Loss-of-function assays, including CCK-8, colony formation assay, flow cytometry analysis and transwell assays, were conducted to verify the effect of SHNG10 on the proliferation, apoptosis, migration and invasion of GC cells. Mechanism experiments were performed to identify the downstream molecular mechanism of SNHG10. Results SNHG10 was expressed at a high level in GC cells. Knockdown of SNHG10 inhibited the proliferation, migration and invasion of GC cells. Silencing of SNHG10 led to the downregulation of core factors of WNT signaling pathway. Knockdown of SNHG10 could decline the expression of CTNNB1 through sequestering miR-495-3p. Conclusions SNHG10 promotes the procession of GC through targeting miR-495-3p/CTNNB1 and activating WNT signaling pathway.

Automated summary

High expression of SNHG10 in GC cells promotes the progression of GC by targeting miR-495-3p/CTNNB1 and activating the WNT signaling pathway.