Ziqi wang , Ruoqing Hou , Shiyu Wang , Min Chen , Dongdong Zheng , Zhiming Zhang , Lu Bai , Cai Chang , Shichong Zhou
{"title":"FGFBP1 promotes triple-negative breast cancer progression through the KLK10-AKT axis","authors":"Ziqi wang , Ruoqing Hou , Shiyu Wang , Min Chen , Dongdong Zheng , Zhiming Zhang , Lu Bai , Cai Chang , Shichong Zhou","doi":"10.1016/j.bbrc.2025.151763","DOIUrl":null,"url":null,"abstract":"<div><div>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.</div></div>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"763 ","pages":"Article 151763"},"PeriodicalIF":2.5000,"publicationDate":"2025-04-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Biochemical and biophysical research communications","FirstCategoryId":"99","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S0006291X25004772","RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q3","JCRName":"BIOCHEMISTRY & MOLECULAR BIOLOGY","Score":null,"Total":0}
引用次数: 0
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.
期刊介绍:
Biochemical and Biophysical Research Communications is the premier international journal devoted to the very rapid dissemination of timely and significant experimental results in diverse fields of biological research. The development of the "Breakthroughs and Views" section brings the minireview format to the journal, and issues often contain collections of special interest manuscripts. BBRC is published weekly (52 issues/year).Research Areas now include: Biochemistry; biophysics; cell biology; developmental biology; immunology
; molecular biology; neurobiology; plant biology and proteomics