Signaling via the CXCR5/ERK pathway is mediated by CXCL13 in mice withbreast cancer

Breast cancer is the most common cause of cancer‑associated mortality andthe most frequently diagnosed type of cancer in women worldwide. It has been revealedthat the chemokine C‑X‑C motif chemokine ligand 13 (CXCL13) serves a pivotal rolein breast cancer growth and is associated with lymph node metastasis. However,to the best of our knowledge, the mechanism by which CXCL13 mediates breast cancergrowth remains uncharacterized. Female BALB/c mice were used in this study. Tumorvolume was calculated and changes of gross tumor morphology were observed by hematoxylinand eosin staining. The expression of CXCL13, C‑X‑C motif chemokine receptor 5(CXCR5) and extracellular signaling‑related kinase (ERK) mRNA and protein expressionwere detected by reverse transcriptase quantitative‑polymerase chain reactionand western blot analysis. Simultaneously, the production of cytokines [interleukin‑1β(IL‑1β), tumor necrosis factor (TNF) and tumor growth factor β1 (TGF‑β1)] wasdetected by an ELISA. The CXCL13 inhibitor reduced tumor volume and growth, andreduced the mRNA and protein expression levels of key members of the CXCR5/ERKsignaling pathway: CXCL13, CXCR5 and ERK. Furthermore, the detectable concentrationof the cytokines IL‑1β and TNF decreased following CXCL13 inhibition, whereasthe concentration of TGF‑β1 was increased. The attenuation of tumor growth resultingfrom CXCL13 inhibition may be associated with the CXCR5/ERK signaling pathway.This study provides a theoretical basis for treating breast cancer through CXCL13inhibition in clinical trials.