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Updated: Jan 21, 2026
08:54
Imaging Spatial Reorganization of a MAPK Signaling Pathway Using the Tobacco Transient Expression System
Published on: March 20, 2016
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FGF5 promotes osteosarcoma cells proliferation via activating MAPK signaling pathway
Dunxin Han1, Mingming Wang2, Zhongkai Yu3
1Department of Spine Surgery, 970 Hospital of the PLA Joint Logistic Support Force, Yantai, Shandong, People's Republic of China.
Cancer Management and Research
|August 3, 2019
Summary
Fibroblast growth factor-5 (FGF5) is overexpressed in osteosarcoma (OS) and drives tumor growth by activating the MAPK pathway. Inhibiting FGF5 shows promise as a therapeutic strategy for OS.
Area of Science:
- Oncology
- Molecular Biology
- Biochemistry
Background:
- Osteosarcoma (OS) is a primary bone malignancy with a high risk of metastasis.
- Understanding the molecular mechanisms driving OS progression is crucial for developing effective therapies.
Purpose of the Study:
- To investigate the role of fibroblast growth factor-5 (FGF5) in osteosarcoma (OS).
- To explore the potential mechanisms by which FGF5 influences OS cell proliferation and tumor growth.
Main Methods:
- Analysis of OS gene expression data from GEO (GSE12865).
- qRT-PCR to detect FGF5 expression in OS tissues and cell lines.
- CRISPR/Cas9 to knockout FGF5; CCK-8 assay and xenograft nude mice for proliferation and tumor growth assessment.
- Western blot to analyze MAPK signaling pathway protein expression.
Main Results:
- FGF5 was significantly upregulated in OS tissues and cells, correlating with poor differentiation, larger tumor size, metastasis, and advanced TNM stage.
- FGF5 knockout inhibited OS cell proliferation and tumor growth in vivo.
- Exogenous FGF5 promoted OS cell proliferation and inhibited apoptosis, while activating the MAPK signaling pathway.
Conclusions:
- FGF5 is overexpressed in OS and promotes proliferation by activating the MAPK signaling pathway.
- FGF5 represents a potential therapeutic target for osteosarcoma.
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