Knockdown of CCNB2 inhibits the tumorigenesis of gastric cancer by regulation of the PI3K/Akt pathway.

Gastric cancer (GC) constitutes a malignant neoplasm with elevated mortality and dismal prognosis, featuring insidious early manifestation, a propensity for recurrence and metastasis, and drug resistance. Hence, there is an exigency to explore novel therapeutic tactics for GC. The expression of Cyclin B2 (CCNB2) is augmented in a multiplicity of human malignancies, nevertheless, investigations into the correlation between CCNB2 and GC are scarce. Our study reveal that CCNB2 is highly expressed in human GC tissues and significantly correlates with unfavorable survival prognoses in GC patients. Functional gain and loss assays demonstrated that CCNB2 can potentiate the proliferation and migration of GC cells both in vitro and in vivo, while its overexpression facilitates the epithelial-mesenchymal transition (EMT) process of GC cells. The outcomes of RNA sequencing imply that CCNB2 is implicated in the activation of the PI3K/AKT signaling pathway. Moreover, overexpression of RHBDL2 can countervail the inhibition of the EMT process and the PI3K/AKT signaling mediated by CCNB2 in GC cells. Thus, targeting this newly identified pathway might constitute a prospective therapeutic strategy for GC.