CCT2 regulates the proliferation, apoptosis, and cell cycle arrest of multiple myeloma cells through the P53 signalling pathway.

Multiple myeloma (MM) is the second most common malignant tumor of the hematologic system, characterized by a high relapse rate and difficulty in achieving a cure. Elucidating the underlying molecular mechanisms driving MM progression is crucial for identifying new therapeutic targets. This study focuses on the molecule CCT2 (Chaperonin Containing TCP1 Subunit 2) to reveal its regulatory role and associated signaling pathway features in the malignant progression of MM. Bioinformatics analyses were used for preliminary screening; correlation analyses with clinical samples assessed its diagnostic value; RT-qPCR and western blot techniques measured expression levels; lentiviral transfection was employed for gene manipulation; CCK8 assays and flow cytometry analyzed cellular behavior; additionally, a subcutaneous xenograft model in nude mice was established for in vivo validation. CCT2 expression was significantly upregulated in the MM patient cohort. Clinical data analysis showed a positive correlation between CCT2 expression and plasma cell proportion, and a negative correlation with patient survival. Functional studies confirmed that CCT2 promotes tumor growth. Knockdown of CCT2 expression via gene silencing markedly activated the p53 signaling pathway, induced apoptosis in MM cells, and caused cell cycle arrest, ultimately inhibiting proliferative capacity. Downregulation of CCT2 effectively activates the p53 signaling pathway, primarily by promoting apoptosis and inducing cell cycle arrest in MM cells, thereby exerting a negative regulatory effect on cell proliferation.