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Status |
Public on Nov 20, 2023 |
Title |
The TGF-β/SMAD pathway upregulates SRC |
Organism |
Homo sapiens |
Experiment type |
Genome binding/occupancy profiling by high throughput sequencing
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Summary |
The non-receptor tyrosine kinase SRC is upregulated in various human cancers and plays crucial roles in cancer progression by promoting invasion and metastasis. We show that the transforming growth factor beta (TGF-β/SMAD pathway directly upregulates SRC during the epithelial-mesenchymal transition. In human epithelial MCF10A cells, TGF-β1 treatment markedly upregulated mRNA expression of SRC. Knockout of SMAD4 suppressed upregulation of SRC by TGF-β1. ChIP-sequencing analysis revealed that SRC was transcribed from the SRC1A promoter, which interacted with SMAD2 and SMAD4, in response to TGF-β1. These findings demonstrate that a direct interaction of the activated SMAD complex with the SRC1A promoter directly upregulates SRC and suggest that TGF-β contributes to SRC upregulation in the tumor microenvironment, where TGF-β-mediated tumor progression takes place.
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Overall design |
MCF10A cells were treated with or without TGF-β1 (10 ng/ml) for 48 h. Fixed lysates were subjected to ChIP using an anti-RNA polymerase II antibody
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Contributor(s) |
Kubo Y, Okuzaki D, Okada M |
Citation(s) |
37439249 |
Submission date |
Nov 26, 2018 |
Last update date |
Nov 21, 2023 |
Contact name |
Daisuke Okuzaki |
E-mail(s) |
dokuzaki@biken.osaka-u.ac.jp
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Phone |
+81-6-6879-4935
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Organization name |
Osaka univ.
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Department |
Immunology Frontier Research Center
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Lab |
Human Immunology (Single Cell Genomics)
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Street address |
Yamadaoka 3-1
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City |
Suita |
State/province |
Osaka |
ZIP/Postal code |
565-0871 |
Country |
Japan |
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Platforms (1) |
GPL16791 |
Illumina HiSeq 2500 (Homo sapiens) |
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Samples (4)
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Relations |
BioProject |
PRJNA506898 |
SRA |
SRP170669 |