ArticleCancer cell2015
14-3-3ζ turns TGF-β's function from tumor suppressor to metastasis promoter in breast cancer by contextual changes of Smad partners from p53 to Gli2.
Article in Cancer cell, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 125 papers.
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Who cites it
125 citing papers in PubMed, 180 citations in OpenAlex.
- LCAL4-FUS cooperation switches on MMP13 and drives osteolytic bone metastasis in breast cancer.Oncogene · 2026Article
- TRIM9-Mediated Degradation of SMAD4 Promotes Pyroptosis and Disruption of the Endothelial Barrier in Aortic Dissection Disease.Cardiovascular toxicology · 2026Article
- How post-translational modifications impact glucocorticoid receptor function in human pathologies.Cell communication and signaling : CCS · 2026Review
- The miR-16-1-3p suppresses proliferation and invasiveness via the MDM2-p53 axis in TGF-β1 signaling in osteosarcoma.Molecular therapy. Oncology · 2026Article
- Doublecortin-like kinase 1 promotes fibroblast activation and fibrotic progression through Smad3 binding in idiopathic pulmonary fibrosis.Journal of biomedical science · 2026Article
- p53 inactivation drives breast cancer metastasis to the brain through SCD1 upregulation and increased fatty acid metabolism.Nature genetics · 2026Article
- New understanding of the molecular pathogenesis and therapeutic progress of hepatocellular carcinoma.Oncology reviews · 2026Review
- Hsa_circ_0016662 acts as a prognostic biomarker and promotes the progression of hepatocellular carcinoma via autophagy regulation.Journal of translational medicine · 2025Article
- Mechanisms of organotropism in breast cancer and predicting metastasis to distant organs using deep learning.Discover oncology · 2025Article
- Proteomic profiling identifies upregulation of aurora kinases causing resistance to taxane-type chemotherapy in triple negative breast cancer.Scientific reports · 2025Article
- TGF-β1/SMAD3-mediated Non-canonical Hedgehog Signaling Promotes Pancreatic Stellate Cell Activation and Fibrosis in Chronic Pancreatitis.International journal of biological sciences · 2025Article
- YY2 Serves as a Novel Prognostic Biomarker Correlated with Immune Microenvironment and Glycolysis in Esophageal Carcinoma.Current genomics · 2025Article
- The Interaction between miRNAs and 14-3-3ζ Protein in Different Diseases.Protein and peptide letters · 2025Review
- Targeting a chemo-induced adaptive signaling circuit confers therapeutic vulnerabilities in pancreatic cancer.Cell discovery · 2024Article
- Versatility of 14-3-3 proteins and their roles in bone and joint-related diseases.Bone research · 2024Review
- CD28 Costimulation Augments CAR Signaling in NK Cells via the LCK/CD3ζ/ZAP70 Signaling Axis.Cancer discovery · 2024Article
- Alterations of ceramide synthesis induce PD-L1 internalization and signaling to regulate tumor metastasis and immunotherapy response.Cell reports · 2024Article
- Analysis of the DNA-binding properties of TGF-β-activated Smad complexes unveils a possible molecular basis for cellular context-dependent signaling.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2024Article
- Pharmacologic Hedgehog inhibition modulates the cytokine profile of osteolytic breast cancer cells.Journal of bone oncology · 2024Article
- Targeting sine oculis homeoprotein 1 (SIX1): A review of oncogenic roles and potential natural product therapeutics.Heliyon · 2024Review
65 more citing papers are in PubMed but not listed here.
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Authors and funding
18 authors at 3 institutions in 3 countries.
Funding
Abstract
Transforming growth factor β (TGF-β) functions as a tumor suppressor in premalignant cells but as a metastasis promoter in cancer cells. The dichotomous functions of TGF-β are proposed to be dictated by different partners of its downstream effector Smads. However, the mechanism for the contextual changes of Smad partners remained undefined. Here, we demonstrate that 14-3-3ζ destabilizes p53, a Smad partner in premalignant mammary epithelial cells, by downregulating 14-3-3σ, thus turning off TGF-β's tumor suppression function. Conversely, 14-3-3ζ stabilizes Gli2 in breast cancer cells, and Gli2 partners with Smads to activate PTHrP and promote TGF-β-induced bone metastasis. The 14-3-3ζ-driven contextual changes of Smad partners from p53 to Gli2 may serve as biomarkers and therapeutic targets of TGF-β-mediated cancer progression.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.