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Published on: June 27, 2017
TGFβ1 enhances MAD1 expression and stimulates promoter-bound Pol II phosphorylation: basic functions of C/EBP, SP and
Nadine Hein1, Kan Jiang, Christian Cornelissen
1Institute of Biochemistry and Molecular Biology, Medical School, RWTH Aachen University, 52057 Aachen, Germany.
Background:
The MAD1 protein, a member of the MYC/MAX/MAD network of transcriptional regulators, controls cell proliferation, differentiation and apoptosis. MAD1 functions as a transcriptional repressor, one direct target gene being the tumor suppressor PTEN. Repression of this gene is critical to mediate the anti-apoptotic function of MAD1. Under certain conditions it also antagonizes the functions of the oncoprotein MYC. Previous studies have demonstrated that MAD1 expression is controlled by different cytokines and growth factors. Moreover we have recently demonstrated that the MAD1 promoter is controlled by the cytokine granulocyte colony-stimulating factor (G-CSF) through the activation of STAT3, MAP kinases and C/EBP transcription factors.
Results:
We observed that in addition to G-CSF, the cytokine transforming growth factor β (TGFβ1) rapidly induced the expression of MAD1 mRNA and protein in promyelocytic tumor cells. Moreover we found that C/EBP and SP transcription factors cooperated in regulating the expression of MAD1. This cooperativity was dependent on the respective binding sites in the proximal promoter, with the CCAAT boxes being bound by C/EBPα/β heterodimers. Both C/EBP and SP transcription factors bound constitutively to DNA without obvious changes in response to TGFβ1. In addition SMAD3 stimulated the MAD1 reporter, cooperated with C/EBPα and was bound to the core promoter region. Thus SMAD3 appears to be a potential link between TGFβ1 signaling and C/EBP regulated promoter activity. Moreover TGFβ1 stimulated the phosphorylation of polymerase II at serine 2 and its progression into the gene body, consistent with enhanced processivity.
Conclusions:
Our findings suggest that C/EBP and SP factors provide a platform of transcription factors near the core promoter of the MAD1 gene that participate in mediating signal transduction events emanating from different cytokine receptors. SMAD3, a target of TGFβ1 signaling, appears to be functionally relevant. We suggest that a key event induced by TGFβ1 at the MAD1 promoter is the recruitment or activation of cofactors, possibly in complex with C/EBP, SP, and SMAD3 transcriptional regulators, that control polymerase activity.
Insights
Transforming growth factor beta 1 (TGFβ1) rapidly induces MAD1 expression by engaging C/EBP and SP transcription factors, with SMAD3 acting as a key mediator. This cytokine signaling pathway regulates cell proliferation and apoptosis through the MAD1 gene.
Area of Science:
- Molecular Biology
- Cell Biology
- Gene Regulation
Background:
- MAD1 protein, a transcriptional repressor in the MYC/MAX/MAD network, regulates cell proliferation, differentiation, and apoptosis.
- MAD1 represses the tumor suppressor PTEN, mediating its anti-apoptotic function and antagonizing the oncoprotein MYC.
- MAD1 expression is controlled by cytokines like granulocyte colony-stimulating factor (G-CSF) via STAT3, MAP kinases, and C/EBP transcription factors.
Purpose of the Study:
- To investigate the role of transforming growth factor beta 1 (TGFβ1) in regulating MAD1 expression.
- To identify transcription factors involved in TGFβ1-mediated induction of MAD1.
- To elucidate the mechanism by which TGFβ1 signaling influences MAD1 gene transcription.
Main Methods:
- Analysis of MAD1 mRNA and protein levels following TGFβ1 treatment in promyelocytic tumor cells.
- Reporter gene assays to assess promoter activity.
- Electrophoretic mobility shift assays (EMSAs) to study transcription factor binding to the MAD1 promoter.
- Co-immunoprecipitation to investigate protein-protein interactions.
- Analysis of RNA polymerase II phosphorylation and progression.
Main Results:
- TGFβ1 rapidly induced MAD1 mRNA and protein expression.
- C/EBP and SP transcription factors cooperated to regulate MAD1 expression, binding to CCAAT boxes and the core promoter region, respectively.
- SMAD3, a TGFβ1 signaling target, stimulated MAD1 reporter activity, cooperated with C/EBPα, and bound to the core promoter.
- TGFβ1 enhanced RNA polymerase II phosphorylation and gene body progression.
Conclusions:
- C/EBP and SP factors form a platform at the MAD1 core promoter for cytokine receptor signaling.
- SMAD3 is a key mediator linking TGFβ1 signaling to C/EBP-regulated MAD1 promoter activity.
- TGFβ1 induces MAD1 expression by recruiting cofactors that modulate polymerase activity, involving C/EBP, SP, and SMAD3.
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