Abstract
In this report, we demonstrated that overexpression of tropomyosin-related kinase B (TrkB) was associated with shorter survival in ovarian cancer patients. Brain-derived neurotrophic factor (BDNF), the TrkB ligand, induced activation (phosphorylation) of TrkB in a dose dependent manner. Besides demonstrating the effect of BDNF/TrkB pathway in enhancing cancer cell migration and invasion but inhibiting apoptosis, we also report for the first time that exogenous hepatocyte growth factor induced TrkB expression at both mRNA and protein levels as well as phosphorylation. Our findings suggest that BDNF/TrkB pathway is important in ovarian carcinogenesis and TrkB may be a potential therapeutic target for ovarian cancer.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Adult
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Aged
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Aged, 80 and over
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Blotting, Western
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Brain-Derived Neurotrophic Factor / biosynthesis*
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Cell Line, Tumor
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Cell Movement / physiology*
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Female
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Gene Silencing
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Hepatocyte Growth Factor / metabolism
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Humans
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Immunohistochemistry
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Immunoprecipitation
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In Situ Nick-End Labeling
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Kaplan-Meier Estimate
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Middle Aged
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Neoplasm Invasiveness / genetics
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Neoplasm Invasiveness / pathology
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Neovascularization, Pathologic / genetics
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Neovascularization, Pathologic / metabolism*
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Ovarian Neoplasms / metabolism*
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Ovarian Neoplasms / mortality
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Ovarian Neoplasms / pathology*
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Prognosis
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RNA, Messenger / analysis
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RNA, Small Interfering
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Receptor, trkB / biosynthesis*
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Reverse Transcriptase Polymerase Chain Reaction
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Vascular Endothelial Growth Factor Receptor-2 / metabolism
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Young Adult
Substances
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Brain-Derived Neurotrophic Factor
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RNA, Messenger
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RNA, Small Interfering
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Hepatocyte Growth Factor
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Receptor, trkB
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Vascular Endothelial Growth Factor Receptor-2