Regulation of Foxe1 by Thyrotropin and Transforming Growth Factor Beta Depends on the Interplay Between Thyroid-Specific, CREB and SMAD Transcription Factors

Thyroid ◽  
2019 ◽  
Vol 29 (5) ◽  
pp. 714-725
Author(s):  
Arístides López-Márquez ◽  
Celia Fernández-Méndez ◽  
Pablo Recacha ◽  
Pilar Santisteban
Keyword(s):  
Transcription Factors ◽  
Growth Factor ◽  
Transforming Growth Factor Beta ◽  
Transforming Growth Factor ◽  
Growth Factor Beta

scholarly journals Transforming Growth Factor Beta has Dual Effects on MMP9 and uPA Expression in HTR-8/SVneo Human Trophoblastic Cell Line

2019 ◽  
Vol 24 (1) ◽  
pp. 26-37
Author(s):  
Sandra Susana Novoa Herran ◽  
Mariela Castelblanco ◽  
Myriam Sanchez-Gomez ◽  
Adriana Umaña Pérez
Keyword(s):  
Transcription Factors ◽  
Growth Factor ◽  
Transforming Growth Factor Beta ◽  
In Silico ◽  
Transforming Growth Factor ◽  
In Silico Analysis ◽  
Negative Regulator ◽  
Trophoblast Invasion ◽  
Trophoblastic Cell ◽  
Growth Factor Beta

Invasion of trophoblast into endometrium is vital for successful pregnancy development. MMP9 and uPA are key proteases in this process, but it is still not clear the regulation of its expression by Transforming Growth Factor Beta (TGF-β), known negative regulator of trophoblast invasion. We evaluated the effect of TGF-β on the transcriptional expression of uPA and MMP9 over time, in HTR- /SVneo trophoblast cells cultured with or without 0.5 % fetal bovine serum, via RT qPCR. The involved transcription factors and signaling pathways were analyzed in silico, using Proscan, Enrich, PCViz and WikiPathway. Results showed that that TGF-β regulates the expression of uPA and MMP9. Serum modified the nature of TGF-β’s effects on uPA expression, from negative without serum to positive with it, showing opposite effects on MMP9 expression. In silico analysis evidenced different transcription factors for each protease, some belonging to TGF-β ssignaling pathway, and crosstalk with MAPK and Wnt/β-catenin pathways. The TGF-β ddual role is discussed proposing that serum affects the cellular context. Transcriptional regulation of MMP9 and uPA by TGF-β is differential and depends on serum presence and evaluation time.

Enhanced jun gene expression is an early genomic response to transforming growth factor beta stimulation

1989 ◽  
Vol 9 (3) ◽  
pp. 1255-1262
Author(s):  
L Pertovaara ◽  
L Sistonen ◽  
T J Bos ◽  
P K Vogt ◽  
J Keski-Oja ◽  
...  
Keyword(s):  
Signal Transduction ◽  
Transcription Factors ◽  
Growth Factor ◽  
Transforming Growth Factor Beta ◽  
Transforming Growth Factor ◽  
A549 Cells ◽  
Base Line ◽  
Tgf Beta ◽  
Early Effect ◽  
Growth Factor Beta

Transforming growth factor beta (TGF beta) is a multifunctional polypeptide that regulates proliferation, differentiation, and other functions of many cell types. The pathway of TGF beta signal transduction in cells is unknown. We report here that an early effect of TGF beta is an enhancement of the expression of two genes encoding serum- and phorbol ester tumor promoter-regulated transcription factors: the junB gene and the c-jun proto-oncogene, respectively. This stimulation was observed in human lung adenocarcinoma A549 cells which were growth inhibited by TGF beta, AKR-2B mouse embryo fibroblasts which were growth stimulated by TGF beta, and K562 human erythroleukemia cells, which were not appreciably affected in their growth by TGF beta. The increase in jun mRNA occurred with picomolar TGF beta concentrations within 1 h of TGF beta stimulation, reached a peak between 1 and 5 h in different cells, and declined gradually to base-line levels. This mRNA response was followed by a large increase in the biosynthesis of the c-jun protein (AP-1), as shown by metabolic labeling and immunoprecipitation analysis. However, differential and cell type-specific regulation appeared to determine the timing and magnitude of the response of each jun gene in a given cell. In AKR-2B and NIH 3T3 cells, only junB was induced by TGF beta, evidently in a protein synthesis-independent fashion. The junB response to TGF beta was maintained in c-Ha-ras and neu oncogene-transformed cells. Thus, one of the earliest genomic responses to TGF beta may involve nuclear signal transduction and amplification by the junB and c-jun transcription factors in concert with c-fos, which is also induced. The differential activation of the jun genes may explain some of the pleiotropic effects of TGF beta.

scholarly journals The Transcription Factors Snail and Slug Activate the Transforming Growth Factor-Beta Signaling Pathway in Breast Cancer

PLoS ONE ◽  
2011 ◽  
Vol 6 (10) ◽  
pp. e26514 ◽  
Author(s):  
Archana Dhasarathy ◽  
Dhiral Phadke ◽  
Deepak Mav ◽  
Ruchir R. Shah ◽  
Paul A. Wade
Keyword(s):  
Breast Cancer ◽  
Transcription Factors ◽  
Growth Factor ◽  
Signaling Pathway ◽  
Transforming Growth Factor Beta ◽  
Transforming Growth Factor ◽  
Growth Factor Beta

scholarly journals Enhanced jun gene expression is an early genomic response to transforming growth factor beta stimulation.

1989 ◽  
Vol 9 (3) ◽  
pp. 1255-1262 ◽  
Author(s):  
L Pertovaara ◽  
L Sistonen ◽  
T J Bos ◽  
P K Vogt ◽  
J Keski-Oja ◽  
...  
Keyword(s):  
Signal Transduction ◽  
Transcription Factors ◽  
Growth Factor ◽  
Transforming Growth Factor Beta ◽  
Transforming Growth Factor ◽  
A549 Cells ◽  
Base Line ◽  
Tgf Beta ◽  
Early Effect ◽  
Growth Factor Beta

Transforming growth factor beta (TGF beta) is a multifunctional polypeptide that regulates proliferation, differentiation, and other functions of many cell types. The pathway of TGF beta signal transduction in cells is unknown. We report here that an early effect of TGF beta is an enhancement of the expression of two genes encoding serum- and phorbol ester tumor promoter-regulated transcription factors: the junB gene and the c-jun proto-oncogene, respectively. This stimulation was observed in human lung adenocarcinoma A549 cells which were growth inhibited by TGF beta, AKR-2B mouse embryo fibroblasts which were growth stimulated by TGF beta, and K562 human erythroleukemia cells, which were not appreciably affected in their growth by TGF beta. The increase in jun mRNA occurred with picomolar TGF beta concentrations within 1 h of TGF beta stimulation, reached a peak between 1 and 5 h in different cells, and declined gradually to base-line levels. This mRNA response was followed by a large increase in the biosynthesis of the c-jun protein (AP-1), as shown by metabolic labeling and immunoprecipitation analysis. However, differential and cell type-specific regulation appeared to determine the timing and magnitude of the response of each jun gene in a given cell. In AKR-2B and NIH 3T3 cells, only junB was induced by TGF beta, evidently in a protein synthesis-independent fashion. The junB response to TGF beta was maintained in c-Ha-ras and neu oncogene-transformed cells. Thus, one of the earliest genomic responses to TGF beta may involve nuclear signal transduction and amplification by the junB and c-jun transcription factors in concert with c-fos, which is also induced. The differential activation of the jun genes may explain some of the pleiotropic effects of TGF beta.

scholarly journals Transforming growth factor-beta and Forkhead box O transcription factors as cardiac fibroblast regulators

2017 ◽  
Vol 11 (2) ◽  
pp. 154-162 ◽  
Author(s):  
Ignacio Norambuena-Soto ◽  
Constanza Núñez-Soto ◽  
Fernanda Sanhueza-Olivares ◽  
Nicole Cancino-Arenas ◽  
David Mondaca-Ruff ◽  
...  
Keyword(s):  
Transcription Factors ◽  
Growth Factor ◽  
Transforming Growth Factor Beta ◽  
Transforming Growth Factor ◽  
Cardiac Fibroblast ◽  
Forkhead Box ◽  
Growth Factor Beta
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