FGFBP1 promotes triple-negative breast cancer progression through the KLK10-AKT axis
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View abstract on PubMed
Summary
This summary is machine-generated.Fibroblast growth factor binding protein 1 (FGFBP1) promotes triple-negative breast cancer (TNBC) growth and spread. Targeting FGFBP1 may offer a new therapeutic strategy for TNBC by inhibiting the KLK10-AKT pathway.
Area Of Science
- Oncology
- Molecular Biology
Background
- Triple-negative breast cancer (TNBC) is aggressive and lacks targeted therapies.
- The fibroblast growth factor (FGF) pathway is implicated in TNBC progression.
- FGFBP1 releases FGFs, but its role in TNBC is unclear.
Purpose Of The Study
- To investigate the role of FGFBP1 in TNBC progression.
- To elucidate the molecular mechanism by which FGFBP1 affects TNBC.
Main Methods
- In vitro and in vivo experiments using TNBC cell lines.
- Analysis of FGFBP1, KLK10, and AKT pathway expression.
- Gene knockdown and pathway inhibition studies.
Main Results
- FGFBP1 overexpression enhanced TNBC cell proliferation, migration, and invasion.
- FGFBP1 upregulated KLK10, activating the AKT pathway.
- Knocking down FGFBP1 or KLK10, or inhibiting AKT, reversed these effects.
Conclusions
- FGFBP1 promotes TNBC progression via the KLK10-AKT axis.
- Targeting FGFBP1 represents a potential therapeutic strategy for TNBC.
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