Abstract
The current study investigated the functional role of long non-coding RNA SNHG14 (lncRNA SNHG14) in gastric cancer (GC) progression and its underlying mechanisms. Compared with para-carcinoma tissues, SNHG14 was upregulated in GC tissues, correlating with a poor prognosis in GC patients. SNHG14 knockdown significantly weakened the proliferation, migration and invasion capabilities of GC cell lines while enhancing the apoptosis ability of GC cells. Simultaneously, SNHG14 overexpression reversed these effects. RNA fluorescence in situ hybridization (FISH) and nucleocytoplasmic separation assays revealed that SNHG14 was primarily located in the cytoplasm of GC cells. Combined sequencing of the miRNAome and transcriptome depicted that miR-206 could be a potential target for SNHG14. Mechanistically, assays such as luciferase reporter, RNA immunoprecipitation (RIP) and RNA pulldown established that lncRNA SNHG14 acted as a sponge for miR-206. This prevented the degradation of its target gene, FNDC3A, playing a tumour-suppressive role in GC. In addition, FNDC3A directly interacted with the SNHG14 promoter and induced transcription, thus facilitating GC progression. Therefore, our research findings suggested a novel pathway to promote GC progression through the FNDC3A/lncRNA SNHG14/miR-206/FNDC3A axis. Moreover, the findings indicated that SNHG14 could become a potential biomarker and therapeutic target for GC.