Conditional ablation of TGF-β signaling inhibits tumor progression and invasion in an induced mouse bladder cancer model.

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.

• Authors: Yu Liang, Fengyu Zhu, Haojie Zhang, Demeng Chen, Xiuhong Zhang, Qian Gao, Yang Li
• Journal: Scientific reports (Sci Rep) Vol. 6 Pg. 29479 (07 05 2016) ISSN: 2045-2322 [Electronic] England
• PMID: 27378170 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)

Chemical References

• Receptors, Transforming Growth Factor beta
• Tgfb1 protein, mouse
• Transforming Growth Factor beta1
• Protein Serine-Threonine Kinases
• Receptor, Transforming Growth Factor-beta Type I

Topics

• Animals
• Apoptosis
• Cell Proliferation
• Disease Models, Animal
• Disease Progression
• Epithelial-Mesenchymal Transition
• Gene Expression Profiling
• Male
• Mice
• Mice, Knockout
• Neoplasm Invasiveness
• Neoplastic Stem Cells (cytology)
• Phosphorylation
• Protein Serine-Threonine Kinases (genetics, metabolism)
• Receptor, Transforming Growth Factor-beta Type I
• Receptors, Transforming Growth Factor beta (genetics, metabolism)
• Signal Transduction
• Transforming Growth Factor beta1 (genetics, metabolism)
• Urinary Bladder Neoplasms (metabolism)