Lysine (K)-specific demethylase 2B (KDM2B) has been testified to be an oncogene in diverse cancers, which joins in mediating the carcinogenesis of cancers. Nonetheless, the function of KDM2B in colon cancer remains unexplored. The study attempted to disclose the influences of KDM2B acetylation in the progression of colon cancer.SW48 and SUN-C1 cells were transfected with Flag-KDM2B and administrated by trichostatin A and nicotinamide for 24 hr. Immunoprecipitation with a Flag antibody followed by western blot with acetyl-lysine-specific antibody was executed to detect KDM2B acetylation. The correlation between CREB binding protein (CBP) and KDM2B was then investigated. The K-R and K-Q mutants were constructed and the impacts of KDM2B on demethylation of nucleosomal substrates, p21, and puma transcription and the carcinogenesis of colon cancer were probed. CBP immediately evoked KDM2B acetylation at lysine residue 765 in colon cancer cells. Acetylation of KDM2B obviously destroyed the relevance with nucleosomes, demethylation of nucleosomal substrates, and repressed p21 and puma transcription. More important, KDM2B acetylation restrained SUN-C1 cells proliferation and colony formation, meanwhile, hindered cell migration and invasion. Beyond that, the tumor formation was repressed by KDM2B acetylation. The observations testified that CBP-triggered KDM2B acetylation accelerated the carcinogenesis of colon cancer. K E Y W O R D S acetylation, colon cancer, CREB binding protein, lysine (K)-specific demethylase 2B

MicroRNA (miR)-126 is known to inhibit inflammatory responses in various inflammatory-related diseases, but its role during the cerebral ischemia/reperfusion (I/R) injury remains unknown. The present study aimed to examine the interaction between miR-126 and RAB3A interacting protein (RAB3IP), and explore its potential protective effects during I/R injury. The human neuroblastoma cell line SH-SY5Y was cultured in an oxygen-glucose deprivation/reoxygenation (OGD/R) environment to simulate I/R injury to assess miR-126 expression and cell viability. SH-SY5Y cells cultured in normal conditions were used as a negative control (NC) group. SH-SY5Y cells were transfected with a miR-126 mimic or an NC mimic, then cultured in OGD/R conditions; in rescue experiments, SH-SY5Y cells were co-transfected with RAB3IP overexpression or NC plasmid together with mimic-NC or mimic-miR, and then maintained in an OGD/R environment to evaluate miR-126, RAB3IP expression, cell viability and apoptosis. Cell viability was reduced in the Model group compared with the NC group, suggesting the successful construction of the OGD/R model. miR-126 expression was downregulated in the Model group compared with the NC group. However, following transfection with mimic-miR, cell viability increased compared with the mimic-NC group. Annexin V and PI staining and Hoechst/PI assays also indicated that apoptosis was reduced in the mimic-miR group compared with the mimic-NC group. RAB3IP expression was reduced following mimic-miR transfection. In rescue experiments, miR-126 negatively regulated RAB3IP expression; by contrast, RAB3IP did not affect that of miR-126. In addition, RAB3IP overexpression attenuated the protective effect of miR-126 on OGD/R-induced apoptosis. These findings suggest that miR-126 protects against cerebral I/R injury by targeting RAB3IP.