RESUMEN

OBJECTIVE: Colorectal cancer (CRC) is a malignant tumor commonly found in the digestive tract. This study aimed to explore the effect of circRNA_002178 as a competing endogenous RNA in the development of CRC by regulating the miR-542-3p/cAMP response element binding protein 1 (CREB1) axis and its molecular mechanism. METHODS: The relative expressions of circ_002178, miR-542-3p, and CREB1 in patients' cell lines and CRC tissues were measured using Western blot and qRT-PCR. The localization and expression of circ_002178 were determined using fluorescence in situ hybridization and nucleocytoplasmic separation tests. The targeting relationships among circ_002178, miR-542-3p, and CREB1 were validated using RNA immunoprecipitation and dual luciferase reporter assays. The cells' proliferation, invasion, and colony forming ability were tested using CCK8, Transwell, and Clone formation assays, respectively. The cellular glucose consumption, lactification, and adenosine triphosphate (ATP) production were measured using glucose uptake colorimetric assay kits, lactate colorimetric assay kits and ATP assay kits, respectively. RESULTS: The circ_002178 and CREB1 expressions were up-regulated in the CRC cells and tissues, and the miR-542-3p expression was down-regulated (all P<0.05). The circ_002178 knockdown inhibited the proliferation, invasion, colony formation, and glycolysis of the CRC cells in vitro, but the overexpression of circ_002178 induced the opposite result (both P<0.05). Our molecular mechanism study revealed that circ_002178, as the molecular sponge of miR-542-3p, promotes CREB1 expression. The downregulation of miR-542-3p or the overexpression of CREB1 is able to partly weaken the inhibition of CRC cells through the circ_002178 knockdown. CONCLUSION: circ_002178 promotes the invasion, proliferation, colony formation, and glycolysis of CRC cells by regulating the miR-542-3p/CREB1 axis, thus driving the development of CRC.