Tumor-derived lactate fuels the STAT3-LCN2 pathway to promote bladder cancer malignancy and chemoresistance.

ABSTRACT: Bladder cancer progression is closely linked to metabolic changes within the tumor microenvironment (TME), particularly elevated lactate levels. Lipocalin 2 (LCN2), a protein involved in iron regulation, has been implicated in tumor progression in several cancers, but its regulatory mechanisms and role in bladder cancer remain unclear. Bladder cancer cell lines were treated with exogenous lactate or subjected to inhibition of endogenous lactate production to evaluate changes in LCN2 expression. The role of Signal Transducer and Activator of Transcription 3 (STAT3) was assessed using genetic knockdown and pharmacological inhibitors. Functional assays including migration, epithelial-to-mesenchymal transition (EMT), sphere formation, and stemness marker analysis were performed to determine th

SUBMITTER: Yu SY 

PROVIDER: S-EPMC12644603 | biostudies-literature | 2025 Nov

REPOSITORIES: biostudies-literature