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Article Abstract
Triple-negative breast cancer (TNBC) is highly malignant, with rapid tumor growth and metastasis. Due to ER-, PR- and HER2-of TNBC, FGFR pathway play a pivotal role in the progression of TNBC. Its ligand FGFs is mostly released from the extracellular matrix by fibroblast growth factor binding protein 1 (FGFBP1). However, little is known about the role of FGFBP1 in TNBC. In this study, we found that overexpression of FGFBP1 significantly promoted the proliferation, migration and invasion of TNBC cells in vitro and in vivo and vice versa. Mechanistically, overexpression of FGFBP1 upregulated the expression of KLK10, thereby activating AKT, which led to proliferation, migration and invasion of TNBC cells. After knocking down FGFBP1, the expression of KLK10 was reduced and the AKT pathway was inhibited. In addition, knocking down KLK10 or inhibiting AKT pathway impaired the promotion effect of overexpression of FGFBP1 on the proliferation and invasion of TNBC cells. These results suggest that FGFBP1 may promote the proliferation, migration and invasion of TNBC cells through the KLK10-AKT axis. Targeting FGFBP1 may serve as a new therapeutic strategy for TNBC.
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