LncRNA SPRY4-IT1 regulates cell proliferation and migration by sponging miR-101-3p and regulating AMPK expression in gastric cancer

Abstract Increasing evidence indicates that long non-coding RNA SPRY4 intronic transcript 1 (lncRNA SPRY4-IT1 ) has been reported to be associated with the progression of several cancers, but its expression level and the function of SPRY4-IT1 in the progression of gastric cancer (GC) have been rarely reported. Here, we reported that SPRY4-IT1 was upregulated in GC. In vitro experiments revealed that SPRY4-IT1 knockdown significantly inhibited GC cells proliferation by causing G1 arrest and promoting apoptosis, whereas SPRY4-IT1 overexpression promoted cell growth. Further functional assays indicated that SPRY4-IT1 overexpression significantly promoted cell migration and invasion. Bioinformatics analysis predicted that there is a SPRY4-IT1/miR-101-3p/AMPK axis in GC progression. Dual-luciferase reporter system validated the direct interaction of SPRY4-IT1, miR-101-3p, and AMPK. Western blot verified that inhibition of SPRY4-IT1 decreased AMPK expression. Furthermore, silencing SPRY4-IT1 suppressed GC growth in vivo . Importantly, we demonstrated that SPRY4-IT1 was upregulated in serum exosomes from GC patients, and correlated with cancer metastasis. Altogether, silencing SPRY4-IT1 suppresses progression of GC by interacting with miR-101-3p and decreasing inhibiting AMPK expression. Taken together, our study demonstrates that SPRY4-IT1 could act as a functional oncogene in GC, as well as a potential therapeutic target for GC patients.