Overexpression of miR-222-3p Promotes the Proliferation and Inhibits the Apoptosis of Diffuse Large B-Cell Lymphoma Cells via Suppressing PPP2R2A.

This study aimed to investigate the effects of microRNA-222-3p on activated B cell-like-type diffuse large B-cell lymphoma cells and the regulatory relationship between microRNA-222-3p and phosphatase 2 regulatory subunit B alpha. The expression of microRNA-222-3p was detected in activated B cell-like-type diffuse large B-cell lymphoma tissues and cells by quantitative reverse transcription polymerase chain reaction. The regulatory effects of microRNA-222-3p on the proliferation, invasion, and apoptosis of activated B cell-like-type diffuse large B-cell lymphoma cells were analyzed by 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide (MTT), colony formation, flow cytometry, and Transwell assay. The regulatory relationship between microRNA-222-3p and phosphatase 2 regulatory subunit B alpha was determined by luciferase reporter gene and RNA pull-down assay. In addition, the effects of microRNA-222-3p on tumor growth were further analyzed in mice. MicroRNA-222-3p and phosphatase 2 regulatory subunit B alpha were significantly up- and downregulated in activated B cell-like-type diffuse large B-cell lymphoma tissues and cells, respectively. Phosphatase 2 regulatory subunit B alpha was a target of microRNA-222-3p. MicroRNA-222-3p promoted the proliferation and invasion and inhibited the apoptosis of activated B cell-like-type diffuse large B-cell lymphoma cells. Phosphatase 2 regulatory subunit B alpha reversed the tumor-promoting effects of microRNA-222-3p on activated B cell-like-type diffuse large B-cell lymphoma cells. In addition, microRNA-222-3p promoted the tumor growth in mice and downregulated phosphatase 2 regulatory subunit B alpha in tumor tissues. MicroRNA-222-3p promoted the proliferation and invasion and inhibited the apoptosis of activated B cell-like-type diffuse large B-cell lymphoma cells through suppressing phosphatase 2 regulatory subunit B alpha expression.