LTF regulates glioblastoma progression and temozolomide resistance via the NF-κB signaling pathway.

Abstract

Glioblastoma (GBM) is the most prevalent tumor in the central nervous system in adults. Lactotransferrin (LTF) is a molecule involved in the growth of various tumors. However, the underlying mechanism of LTF in GBM progression and chemotherapy resistance remains unclear. In this study, the clinical and diagnostic value of LTF were evaluated. In vitro and in vivo experiments were performed to explore the functional role of LTF in GBM. Immunoprecipitation and immunofluorescence assays were performed to clarify the effect of LTF on nuclear factor-κB (NF-κB) activation. LTF was overexpressed in GBM and correlated with poor prognosis. LTF promoted GBM cell proliferation, invasion, and temozolomide (TMZ) resistance. Mechanism assay results indicated that LTF competitively binds to p65, rescuing the inhibited effect of PP2A on p65 phosphorylation, thereby activating the NF-κB signaling pathway. Our results confirmed that highly expressed LTF promoted GBM progression and TMZ resistance through the NF-κB signaling pathway.