Abstract
The role of transforming growth factor-β (TGF-β) signaling in cancer progression is still under debate. To determine the function of TGF-β signaling in bladder cancer progression, we conditionally knocked out the Tgfbr2 in mouse model after a N-butyl-N-4-hydroxybutyl Nitrosamine induced bladder carcinogenesis. We found the ablation of TGF-β signaling could inhibit the cancer cell proliferation, cancer stem cell population and EMT, hence suppressed the invasive cancer progression, which is similar with the result of TGF-β receptor I inhibitor treatment. These findings recognize the roles and mechanisms of TGF-β signaling in bladder cancer progression in vivo for the first time.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Apoptosis
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Cell Proliferation
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Disease Models, Animal
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Disease Progression*
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Epithelial-Mesenchymal Transition
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Gene Expression Profiling
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Male
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Mice
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Mice, Knockout
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Neoplasm Invasiveness
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Neoplastic Stem Cells / cytology
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Phosphorylation
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Protein Serine-Threonine Kinases / genetics
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Protein Serine-Threonine Kinases / metabolism*
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Receptor, Transforming Growth Factor-beta Type I
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Receptors, Transforming Growth Factor beta / genetics
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Receptors, Transforming Growth Factor beta / metabolism*
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Signal Transduction
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Transforming Growth Factor beta1 / genetics
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Transforming Growth Factor beta1 / metabolism*
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Urinary Bladder Neoplasms / metabolism*
Substances
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Receptors, Transforming Growth Factor beta
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Tgfb1 protein, mouse
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Transforming Growth Factor beta1
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Protein Serine-Threonine Kinases
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Receptor, Transforming Growth Factor-beta Type I