ArticleOncotarget2016
Twist1 induces distinct cell states depending on TGFBR1-activation.
Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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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.
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Who cites it
8 citing papers in PubMed, 17 citations in OpenAlex.
- Complex aberrant expression of planar nuclear polarity factors in intraductal papillary mucinous neoplasm of the pancreas.Virchows Archiv : an international journal of pathology · 2026Article
- A computational approach for perturbation-induced EMT transitions.NPJ systems biology and applications · 2025Article
- The activation of EP300 by F11R leads to EMT and acts as a prognostic factor in triple-negative breast cancers.The journal of pathology. Clinical research · 2023Article
- Expressions of TWIST1 and CD105 markers in colorectal cancer patients and their association with metastatic potential and prognosis.Diagnostic pathology · 2021Article
- Plasticity of cancer cell invasion: Patterns and mechanisms.Translational oncology · 2021Review
- Systems biology approach suggests new miRNAs as phenotypic stability factors in the epithelial-mesenchymal transition.Journal of the Royal Society, Interface · 2020Article
- ETS1 regulates Twist1 transcription in a KrasClinical & experimental metastasis · 2018Article
- miR-320 inhibited ovarian cancer oncogenicity via targeting TWIST1 expression.American journal of translational research · 2017Article
Corrections and comments
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Authors and funding
12 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Basic helix-loop-helix transcription factor Twist1 is a master regulator of Epithelial-Mesenchymal Transition (EMT), a cellular program implicated in different stages of development as well as metastatic dissemination of carcinomas. Here, we show that Twist1 requires TGF-beta type-I receptor (TGFBR1)-activation to bind an enhancer region of downstream effector ZEB1, thereby inducing ZEB1 transcription and EMT. When TGFBR1-phosphorylation is inhibited, Twist1 generates a distinct cell state characterized by collective invasion, simultaneous proliferation and expression of endothelial markers. By contrast, TGFBR1-activation directs Twist1 to induce stable mesenchymal transdifferentiation through EMT, thereby generating cells that display single-cell invasion, but lose their proliferative capacity. In conclusion, preventing Twist1-induced EMT by inhibiting TGFβ-signaling does not generally block acquisition of invasion, but switches mode from single-cell/non-proliferative to collective/proliferative. Together, these data reveal that transient Twist1-activation induces distinct cell states depending on signaling context and caution against the use of TGFβ-inhibitors as a therapeutic strategy to target invasiveness.
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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.