IL-1β Controls Proliferation, Apoptosis, and Necroptosis Through the PI3K/AKT/NF-κB Pathway in Leukaemic Lymphoblasts

Chronic inflammation and the development of cancer are closely linked, with components that comprise the tumour microenvironment—including proinflammatory cytokines—exerting essential tumourigenic effects. These proinflammatory cytokines include IL-1β, which has been reported to be overexpressed in several cancers and shown to activate several signalling pathways. These pathways may involve kinases such as AKT and Src, and have a broad capacity to activate nuclear factors, including NF-κB, which can regulate the transcription of genes encoding proteins such as cIAP1, Bcl-2, and cyclin D, thereby regulating processes like apoptosis and cell cycle inhibition. The objective of this study was to investigate the role of IL-1β in regulating cell death and proliferation in leukaemic lymphoblasts via the PI3K/AKT/NF-κB pathway. We employed flow cytometry to determine the expression levels and phosphorylation status of various proteins, proliferation was assessed using the CCK-8 kit, and apoptosis was evaluated with the Annexin V kit. Our findings indicate that the signalling pathway activated by IL-1β modulates these cellular processes in leukaemic lymphoblasts. We therefore conclude that IL-1β exerts significant effects on cell death and proliferation in leukaemic lymphoblasts through the PI3K/AKT/NF-κB pathway, with the study’s findings indicating that an inflammatory environment may promote such lymphoblasts to acquire neoplastic characteristics. As such, the proteins involved in the effects evaluated in this work could be considered as potential therapeutic targets for the treatment of Acute Lymphoblastic Leukaemia (ALL).