Circular RNA circ_C16orf62 Suppresses Cell Growth in Gastric Cancer by miR-421/Tubulin beta-2A Chain (TUBB2A) Axis.

BACKGROUND Gastric cancer (GC) is the third leading cause of cancer-associated mortality in the world. Expression of circular RNA circ_C16orf62 is reported to be low in GC. The role and mechanism of circ_C16orf62 remain unclear. MATERIAL AND METHODS Expression levels of circ_C16orf62 and tubulin beta-2A chain (TUBB2A) in GC tissues and cells, and microRNA-421 (miR-421) level in GC cells were detected by real-time quantitative polymerase chain reaction (RT-qPCR). The predominant cytoplasmic localization of circ_C16orf62 was identified by subcellular fractionation. The protein level of TUBB2A was detected by western blot assay. Cell proliferative ability, migration, and invasion were measured by 3-(4, 5-dimethyl-2-thiazolyl)-2, 5-diphenyl-2-H-tetrazolium bromide (MTT), colony formation, and several transwell assaysy. The binding relationship between miR-421 and circ_C16orf62 or TUBB2A was predicted by starBase3.0 or Targetscan, and then verified by the dual-luciferase reporter assay. The biological role ofcirc_C16orf62 was examined by xenograft tumor model in vivo. RESULTS Circ_C16orf62 andTUBB2A were downregulated in GC tissues and cells. Circ_C16orf62 was predominantly located in the cytoplasm of GC cells, and repressed proliferation, migration, and invasion of GC cells. Mechanistically, circ_C16orf62 worked as the miR-421 sponge to upregulate TUBB2A in GC, thereby hindering GC growth. Circ_C16orf62 repressed GC tumor growth in vivo. CONCLUSIONS These findings demonstrate that circ_C16orf62 impeded proliferation, migration, and invasion in vitro and retarded tumor growth in vivo by the miR-421/TUBB2A axis in GC, providing a potential therapeutic strategy for patients with GC.