scholarly journals Lack of Fetuin-A (α2-HS-Glycoprotein) Reduces Mammary Tumor Incidence and Prolongs Tumor Latency via the Transforming Growth Factor-β Signaling Pathway in a Mouse Model of Breast Cancer

2010 ◽  
Vol 177 (5) ◽  
pp. 2635-2644 ◽  
Author(s):  
Bobby Guillory ◽  
Amos M. Sakwe ◽  
Margret Saria ◽  
Pamela Thompson ◽  
Christine Adhiambo ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Growth Factor ◽  
Mouse Model ◽  
Signaling Pathway ◽  
Mammary Tumor ◽  
Transforming Growth Factor ◽  
Transforming Growth Factor Β ◽  
Tumor Incidence ◽  
Fetuin A

Expression analysis of selected miR‐206 targets from the transforming growth factor‐β signaling pathway in breast cancer

2019 ◽  
Vol 120 (8) ◽  
pp. 13545-13553
Author(s):  
Mahnaz Seifi‐Alan ◽  
Ali Dianatpour ◽  
Lobat Geranpayeh ◽  
Reza Mirfakhraie ◽  
Mir D. Omrani ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Growth Factor ◽  
Signaling Pathway ◽  
Expression Analysis ◽  
Transforming Growth Factor ◽  
Transforming Growth Factor Β

127 TREATMENTS WITH DIVERSE ENDOCRINE-DISRUPTING CHEMICALS RESULTED IN THE INHIBITION OF OVARIAN TUMOR PROGRESSION VIA INTERRUPTION OF TRANSFORMING GROWTH FACTOR-β IN IN VITRO AND XENOGRAFTED MOUSE MODELS

2014 ◽  
Vol 26 (1) ◽  
pp. 177
Author(s):  
H.-R. Lee ◽  
R.-E. Go ◽  
K.-C. Choi
Keyword(s):  
Ovarian Cancer ◽  
Growth Factor ◽  
Mouse Model ◽  
Cancer Cells ◽  
Signaling Pathway ◽  
Mouse Models ◽  
Transforming Growth Factor ◽  
Transforming Growth Factor Β ◽  
Xenograft Mouse Model

Activated oestrogen receptor (ER) signaling pathway by 17β-estadiol (E2) appeared to suppress transforming growth factor β (TGF-β) signaling pathway by cross-talk with TGF-β components in ER-positive cancer cells. In this study, we further examined the inhibitory effects of alkylphenols, including 4-nonylphenol (NP), 4-otylphenol (OP), bisphenol A (BPA), and benzophenon-1 (BP-1), in TGF-β signaling pathway. The transcriptional and translational levels of TGF-β-related genes were examined by reverse-transcription PCR (RT-PCR), Western blotting analysis in xenografted mouse models of ovarian cancer BG-1 cells. The NP, OP, and BPA induced the expression of snoN, a TGF-β pathway inhibitor. Treatment with NP, BPA, and BP-1 resulted in decreased phosphorylation of Smad3, a downstream target of TGF-β. With these 2 effects, NP and BPA stimulated the proliferation of BG-1 cells via inhibition of the TGF-β signaling pathway. In a xenograft mouse model, transplanted BG-1 ovarian cancer cells showed significantly decreased phosphorylation of Smad3 and increased expression of snoN in the ovarian tumour masses following treatment with E2, NP, or BPA. In parallel with an in vitro model, the expressions of TGF-β signaling pathway were similarly regulated by NP or BPA in a xenograft mouse model, revealing consistent results. Taken together, these results support that NP and BPA may cause the disruption of the TGF-β signaling pathway and increase the risk of oestrogen-dependent cancers such as ovarian cancer. This work was supported by a grant from the Next-Generation BioGreen 21 Program (No. PJ009599), Rural Development Administration, Republic of Korea.

scholarly journals Signaling through ShcA Is Required for Transforming Growth Factor β- and Neu/ErbB-2-Induced Breast Cancer Cell Motility and Invasion

2008 ◽  
Vol 28 (10) ◽  
pp. 3162-3176 ◽  
Author(s):  
Jason J. Northey ◽  
Juliann Chmielecki ◽  
Elaine Ngan ◽  
Caterina Russo ◽  
Matthew G. Annis ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Growth Factor ◽  
Cell Motility ◽  
Cancer Cells ◽  
Mammary Tumor ◽  
Breast Cancer Cells ◽  
Transforming Growth Factor ◽  
Adaptor Protein ◽  
Transforming Growth Factor Β ◽  
Migration And Invasion

ABSTRACT Cooperation between the Neu/ErbB-2 and transforming growth factor β (TGF-β) signaling pathways enhances the invasive and metastatic capabilities of breast cancer cells; however, the underlying mechanisms mediating this synergy have yet to be fully explained. We demonstrate that TGF-β induces the migration and invasion of mammary tumor explants expressing an activated Neu/ErbB-2 receptor, which requires signaling from autophosphorylation sites located in the C terminus. A systematic analysis of mammary tumor explants expressing Neu/ErbB-2 add-back receptors that couple to distinct signaling molecules has mapped the synergistic effect of TGF-β-induced motility and invasion to signals emanating from tyrosine residues 1226/1227 and 1253 of Neu/ErbB-2. Given that the ShcA adaptor protein is known to interact with Neu/ErbB-2 through these residues, we investigated the importance of this signaling molecule in TGF-β-induced cell motility and invasion. The reduction of ShcA expression rendered cells expressing activated Neu/ErbB-2, or add-back receptors signaling specifically through tyrosines 1226/1227 or 1253, unresponsive to TGF-β-induced motility and invasion. In addition, a dominant-negative form of ShcA, lacking its three known tyrosine phosphorylation sites, completely abrogates the TGF-β-induced migration and invasion of breast cancer cells expressing activated Neu/ErbB-2. Our results implicate signaling through the ShcA adaptor as a key component in the synergistic interaction between these pathways.

scholarly journals Bone Sialoprotein Mediates the Tumor Cell–Targeted Prometastatic Activity of Transforming Growth Factor β in a Mouse Model of Breast Cancer

2006 ◽  
Vol 66 (12) ◽  
pp. 6327-6335 ◽  
Author(s):  
Jeong-Seok Nam ◽  
Adam M. Suchar ◽  
Mi-Jin Kang ◽  
Christina H. Stuelten ◽  
Binwu Tang ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Growth Factor ◽  
Mouse Model ◽  
Tumor Cell ◽  
Transforming Growth Factor ◽  
Transforming Growth Factor Β ◽  
Bone Sialoprotein

scholarly journals Combined Genetic Assessment of Transforming Growth Factor-β Signaling Pathway Variants May Predict Breast Cancer Risk

2005 ◽  
Vol 65 (8) ◽  
pp. 3454-3461 ◽  
Author(s):  
Virginia G. Kaklamani ◽  
Lisa Baddi ◽  
Junjian Liu ◽  
Diana Rosman ◽  
Sharbani Phukan ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Growth Factor ◽  
Breast Cancer Risk ◽  
Cancer Risk ◽  
Signaling Pathway ◽  
Transforming Growth Factor ◽  
Transforming Growth Factor Β ◽  
Genetic Assessment

Versican G1 and G3 domains are upregulated and latent transforming growth factor-β binding protein-4 is downregulated in breast cancer stroma

Breast Cancer ◽  
2011 ◽  
Vol 19 (1) ◽  
pp. 46-53 ◽  
Author(s):  
Yuko Takahashi ◽  
Hiroko Kuwabara ◽  
Masahiko Yoneda ◽  
Zenzo Isogai ◽  
Nobuhiko Tanigawa ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Growth Factor ◽  
Transforming Growth Factor ◽  
Binding Protein ◽  
Transforming Growth Factor Β ◽  
Cancer Stroma
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