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.
Highlights
The TGF-βsignaling pathway is involved in various aspects of psychological and physiological processes, including genesis and progression of urinary bladder cancer[26,27]
It has been shown that TGF-β1 secretion levels correlates with more aggressive phenotype of bladder cancer cell lines[28]
We set off to define the role of TGF-βsignaling pathway in bladder cancer invasion in vivo
Summary
TGF-β signaling is required for BBN-induced invasive bladder cancer progression. Four weeks after Tamoxifen administration, tumors from both control and conditional Tgfbr[2] knockout mice were collected for further analysis (Fig. 2A). Immunohistochemistry analysis revealed strong phosphorylation of Smad[2] of Ser465/467, which is an activation marker of TGF signaling[18], in control invasive cancer cells.
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