ArticleNucleic acids research2018
JUNB governs a feed-forward network of TGFβ signaling that aggravates breast cancer invasion.
Article in Nucleic acids research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 76 papers.
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Who cites it
76 citing papers in PubMed, 117 citations in OpenAlex.
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- Defining the Tumor-Bone axis: the role of extracellular vesicles in a crucial exchange route for breast cancer development and progression.Clinical & experimental metastasis · 2025Review
- Integrative analysis of circulating tumor cells (CTCs) and exosomes from small-cell lung cancer (SCLC) patients: a comprehensive approach.Molecular oncology · 2025Article
- JunB-HBZ nuclear translocation by TGF-β is a key driver in HTLV-1-mediated leukemogenesis.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Dasatinib and quercetin senolytic treatment delays early onset intervertebral disc degeneration in SM/J mice.Research square · 2025Article
- Transparent 3-Layered Bacterial Nanocellulose as a Multicompartment and Biomimetic Scaffold for Co-Culturing Cells.Journal of functional biomaterials · 2025Article
- Transcription factor JUNB is required for transformation of EpCAM-positive hepatocellular carcinoma (HCC) cells into CD90-positive HCC cells in vitro.Cell death & disease · 2025Article
- Minimally invasive determination of pancreatic ductal adenocarcinoma (PDAC) subtype by means of circulating cell-free RNA.Molecular oncology · 2025Article
- Triple-Negative Breast Cancer Progression and Drug Resistance in the Context of Epithelial-Mesenchymal Transition.Cancers · 2025Review
- Spatial tumor immune heterogeneity facilitates subtype co-existence and therapy response in pancreatic cancer.Nature communications · 2025Article
- Transcriptional regulators ensuring specific gene expression and decision-making at high TGFβ doses.Life science alliance · 2025Article
- Growth differentiation factor 7 alleviates the proliferation and metastasis of hepatocellular carcinoma.Liver research (Beijing, China) · 2024Article
- Galectin 3-binding protein (LGALS3BP) depletion attenuates hepatic fibrosis by reducing transforming growth factor-β1 (TGF-β1) availability and inhibits hepatocarcinogenesis.Cancer communications (London, England) · 2024Article
16 more citing papers are in PubMed but not listed here.
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Authors and funding
12 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
It is well established that transforming growth factor-β (TGFβ) switches its function from being a tumor suppressor to a tumor promoter during the course of tumorigenesis, which involves both cell-intrinsic and environment-mediated mechanisms. We are interested in breast cancer cells, in which SMAD mutations are rare and interactions between SMAD and other transcription factors define pro-oncogenic events. Here, we have performed chromatin immunoprecipitation (ChIP)-sequencing analyses which indicate that the genome-wide landscape of SMAD2/3 binding is altered after prolonged TGFβ stimulation. De novo motif analyses of the SMAD2/3 binding regions predict enrichment of binding motifs for activator protein (AP)1 in addition to SMAD motifs. TGFβ-induced expression of the AP1 component JUNB was required for expression of many late invasion-mediating genes, creating a feed-forward regulatory network. Moreover, we found that several components in the WNT pathway were enriched among the late TGFβ-target genes, including the invasion-inducing WNT7 proteins. Consistently, overexpression of WNT7A or WNT7B enhanced and potentiated TGFβ-induced breast cancer cell invasion, while inhibition of the WNT pathway reduced this process. Our study thereby helps to explain how accumulation of pro-oncogenic stimuli switches and stabilizes TGFβ-induced cellular phenotypes of epithelial cells.
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