ARAP1-AS1 Overexpression Increases Diffuse Large B Cell Lymphoma Progression by Sponging miR-508-5p to Activate the EMP1-PI3K/AKT Pathway.

Diffuse large B cell lymphoma (DLBCL) is a type of common and fatal non-Hodgkin lymphoma. This study aimed to detect the specific function of lncRNA ARAP1-AS1 in DLBCL. The in vitro experiments were performed using RT-qPCR, western blotting, MTT, colony formation, flow cytometry analysis, FISH, RNA pulldown, and luciferase reporter assays. A xenograft mouse model was used to evaluate tumor growth in vivo. ARAP1-AS1 expression was upregulated in DLBCL tissues and cells. ARAP1-AS1 knockdown inhibited DLBCL cell proliferation and promoted apoptosis. ARAP1-AS1 activated PI3K/AKT signaling by upregulating EMP1 expression via miR-508-5p. EMP1 overexpression markedly abolished the effect of ARAP1-AS1 knockdown on DLBCL cell proliferation and apoptosis, and PI3K inhibitor reversed the effect of ARAP1-AS1 overexpression on DLBCL cells. ARAP1-AS1 knockdown inhibited DLBCL tumor growth and reduced Ki-67, EMP1, and p-AKT expression in xenograft mouse models. ARAP1-AS1 knockdown exerts anti-tumor effect on DLBCL progression through the miR-508-5p/EMP1/PI3K/AKT axis.