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Up-regulated cten by FGF2 contributes to FGF2-mediated cell migration
Shih-Ya Hung1, Yi-Ping Shih, Michelle Chen
1Center for Tissue Regeneration and Repair, Department of Biochemistry and Molecular Medicine, University of California-Davis, Sacramento, California.
Molecular Carcinogenesis
|April 30, 2013
Summary
Cten protein expression increases in many cancers. Growth factors and cytokines up-regulate cten via specific signaling pathways, promoting cancer cell migration and suggesting cten as a therapeutic target.
Area of Science:
- Molecular biology
- Cancer research
- Cell signaling
Background:
- Cten is a focal adhesion molecule.
- Cten is minimally expressed in normal tissues but highly expressed in various cancers.
- Aberrant cten expression suggests a role in tumorigenesis.
Purpose of the Study:
- Investigate mechanisms inducing cten expression.
- Determine the function of up-regulated cten in cancer.
- Identify cten as a potential therapeutic target.
Main Methods:
- Examined effects of growth factors/cytokines on cten expression.
- Analyzed signaling pathways (Mek-Erk, PI3K-Akt, Jak-Stat).
- Investigated cten's role in cell migration using gene silencing and overexpression.
Main Results:
- EGF, FGF2, NGF, PDGF, TGF-β, IGF-1, IL-6, and IL-13 induced cten expression.
- Mek-Erk and PI3K-Akt pathways mediate cten up-regulation.
- Cten silencing reduced cell motility; cten overexpression promoted it.
Conclusions:
- Cten is a common downstream target of cancer-associated growth factors.
- Up-regulated cten modulates growth factor-induced cell migration.
- Cten represents a potential therapeutic target for cancers with aberrant signaling.
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