The promotes gastric cancer cell proliferation, migration, and invasion by sponging to regulate expression.

BACKGROUND

Long non-coding RNAs (lncRNAs) play critical roles in gastric cancer (GC) initiation progression. However, the biological function of the telomerase RNA component () remains unknown in human GC. The present study sought to determine the biological function and underlying molecular mechanism of the in GC progression.

METHODS

The expression levels of the in GC tissues and cell lines were analyzed using reverse transcription-quantitative polymerase chain reaction (RT-qPCR). The effects of the on the proliferation, migration, and invasion of GC cells were determined using Cell Counting Kit-8 (CCK-8) and Transwell assays. Dual luciferase reporter and argonaute 2 (AGO2)-RNA immunoprecipitation (RIP) assays were used to detect the binding between the and microRNA-423-5p (). Western blotting was performed to measure the expression levels of sex determining region Y-box 12 (), , , matrix metallopeptidase 9 (), and proliferating cell nuclear antigen ().

RESULTS

The results demonstrated that the expression levels were upregulated in GC cells and tissues, while expression levels were downregulated. The upregulation of the was associated with a shorter overall survival in patients with GC. The knockdown of the significantly reduced the proliferation, migration, and invasion of human GC cell lines HGC-27 and SNU-1 cells. Further, the knockdown in the HGC-27 and SNU-1 cells significantly downregulated the expression levels of , , , and , and upregulated the expression levels of and . was also identified as a target of the and was found to directly bind to the . Additionally, was found to directly target to inhibit the proliferation, migration, and invasion of the HGC-27 and SNU-1 cells.

CONCLUSIONS

In conclusion, the findings of this study suggested that the may regulate the / signaling axis by directly sponging and inhibiting expression, thereby leading to the progression of GC. These findings may reveal novel targets for future GC therapy.