The long non-coding RNA small nucleolar RNA host gene 12 (SNHG12) has recently been reported to have an oncogenic role in gastric cancer (GC), but the molecular mechanisms remain largely elusive. In the present study, it was observed that SNHG12 was significantly upregulated in GC tissues and cell lines. High expression of SNHG12 was associated with GC progression and poor prognosis of patients. Knockdown of SNHG12 markedly inhibited the proliferation and migration of the BGC823 and HGC27 GC cell lines. MicroRNA (miR)-16 was identified as a target of SNHG12, and its expression was negatively regulated by SNHG12 in BGC823 and HGC27 cells. In addition, the expression of miR-16 was significantly decreased in GC tissues and cell lines, and inversely associated with the expression of SNHG12 in GC tissues. Furthermore, knockdown of miR-16 impaired the inhibitory effects on GC cell proliferation and migration induced by downregulation of SNHG12. In conclusion, the present study demonstrates that inhibition of SNHG12 suppresses GC cell proliferation and migration by modulation of miR-16 expression, and thus suggests that the SNHG12/miR-16 interaction may be used as a promising target for GC treatment.
Keywords: gastric cancer; microRNA-16; migration; proliferation; small nucleolar RNA host gene 12.