ArticleCell2016
TGF-β Tumor Suppression through a Lethal EMT.
Article in Cell, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 383 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
383 citing papers in PubMed, 1 synthesis or guideline pooled it, 599 citations in OpenAlex.
- Association of SMAD4 loss with drug resistance in clinical cancer patients: A systematic meta-analysis.PloS one · 2021Pooled it
- A phase 1b/2 study of first-line anti-PD-L1/ TGF-βRII fusion protein SHR-1701 combined with nab-paclitaxel and gemcitabine for advanced pancreatic ductal adenocarcinoma.Signal transduction and targeted therapy · 2025Trial
- Addition of SHR-1701 to first-line capecitabine and oxaliplatin (XELOX) plus bevacizumab for unresectable metastatic colorectal cancer.Signal transduction and targeted therapy · 2024Trial
- Salvianolic acid monomers against metastasis: Decoding the multilayered interception of EMT, angiogenesis and immune evasion (Review).International journal of molecular medicine · 2026Review
- Oncogenic RAS as an adaptive signaling ecosystem: context-dependent vulnerabilities and resistance-informed therapeutic design.Experimental hematology & oncology · 2026Review
- Multi-stromal organoid co-culture modelling reveals epithelial-fibroblast heterogeneity in pancreatic cancer and pancreatitis.Nature cell biology · 2026Article
- Metabolic control of smooth muscle cell phenotype switching in atherosclerosis.Science advances · 2026Article
- Expression of Transforming Growth Factor Beta 1 in Lung Adenocarcinoma and Its Relationship with Circulating Tumour Cells.Biochemical genetics · 2026Article
- Recombinant bone morphogenetic protein-2 attenuates colorectal cancer progression by orchestrating Hippo pathway activation, Yes-associated protein inhibition, and epithelial-mesenchymal transition suppression.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2026Article
- Article
- PSMC2 serves as a potential regulatory target of EZH2 in promoting glioma progression via epithelial-mesenchymal transition.Scientific reports · 2026Article
- Adipogenic transdifferentiation reprograms EMT-high PDAC cells into a post-mitotic adipocyte-like state and limits metastasis.Cell death & disease · 2026Article
- SOX4 induces cisplatin resistance in cervical cancer cells by inhibiting aerobic glycolysis.Cell death discovery · 2026Article
- Knockdown of SOX4 attenuates sepsis myocardial injury by inhibiting the EZH2/H3K27me3/SOCS3 axis.Mammalian genome : official journal of the International Mammalian Genome Society · 2026Article
- Clinical and immunological implications of lymphocyte-activation gene 3 expression in metastatic colorectal cancer.Cancer immunology, immunotherapy : CII · 2026Article
- CRISPR screen of human pancreatic cancer xenografts identifies a KLF5 proliferation vulnerability through epigenetic modifiers NCAPD2 and MTHFD1.Molecular cancer · 2026Article
- HCMV infection disrupts barrier functions and promotes epithelial-mesenchymal transition in a cholangiocyte organoid model.Nature communications · 2026Article
- Article
- Targeting Tumour Heterogeneity through sequential timing of anti-hallmark combination therapies -a hypothesis for implementation.Frontiers in immunology · 2026Review
- Smad4 and Eomes converge on a shared transcriptional program associated with inflammatory CD8 T-cell differentiation.Frontiers in immunology · 2026Article
323 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
Abstract
TGF-β signaling can be pro-tumorigenic or tumor suppressive. We investigated this duality in pancreatic ductal adenocarcinoma (PDA), which, with other gastrointestinal cancers, exhibits frequent inactivation of the TGF-β mediator Smad4. We show that TGF-β induces an epithelial-mesenchymal transition (EMT), generally considered a pro-tumorigenic event. However, in TGF-β-sensitive PDA cells, EMT becomes lethal by converting TGF-β-induced Sox4 from an enforcer of tumorigenesis into a promoter of apoptosis. This is the result of an EMT-linked remodeling of the cellular transcription factor landscape, including the repression of the gastrointestinal lineage-master regulator Klf5. Klf5 cooperates with Sox4 in oncogenesis and prevents Sox4-induced apoptosis. Smad4 is required for EMT but dispensable for Sox4 induction by TGF-β. TGF-β-induced Sox4 is thus geared to bolster progenitor identity, whereas simultaneous Smad4-dependent EMT strips Sox4 of an essential partner in oncogenesis. Our work demonstrates that TGF-β tumor suppression functions through an EMT-mediated disruption of a lineage-specific transcriptional network.
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What OpenQuestion holds
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.