ReviewCell research2012
Normal and disease-related biological functions of Twist1 and underlying molecular mechanisms.
Review in Cell research, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 290 papers.
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
290 citing papers in PubMed, 458 citations in OpenAlex.
- Article
- Craniofacial development: genetics, signaling pathways, teratogenic mechanisms, and clinal significance.Molecular biomedicine · 2026Review
- FFPE-CUTAC: A Single Assay, Multiple Layers.bioRxiv : the preprint server for biology · 2026Article
- Transcription cofactor Hes6 interacts with Twist1 to facilitate EMT and promote gastric carcinogenesis by activating the PI3K/AKT signaling.Genes & diseases · 2026Article
- Fusion-driven oncogenic programs shape the immune landscape in translocation renal cell carcinoma.Nature communications · 2026Article
- Twist1 overexpression models an aggressive subtype of pancreatic ductal adenocarcinoma in vivo.Lab animal · 2026Article
- Mesothelial Plasticity Specifies Divergent Pleural Immune Circuits that Instruct Lung Regeneration versus Degeneration.Research square · 2026Article
- TWIST1 bridges p53 and MDM2 and impairs the efficacy of MDM2 inhibitors.Journal of experimental & clinical cancer research : CR · 2026Article
- CD147-positive migrasome macropinocytosis promotes HCC sorafenib resistance via inducing vasculogenic mimicry triggered by PI3K/AKT/TWIST1 signaling.Cell death & disease · 2026Article
- Rewiring miR-22/SNAI1 via CRISPR-based edge editing destabilizes the epithelial phenotype.NPJ systems biology and applications · 2026Article
- The role and mechanism by which micropeptide WHPP promote refractory wound healing.Journal of translational medicine · 2026Article
- Fibroblast growth factor signals drive the metastatic behavior in small cell lung cancer.British journal of cancer · 2026Article
- Loss of Twist1 leads to disruption of ciliary length, endocytic vesicle dynamics, and cell-cell junctions during neural tube formation.Developmental dynamics : an official publication of the American Association of Anatomists · 2026Article
- The craniofacial shape of modern humans embodies genomic signatures of evolution, diversity, and clinical conditions.bioRxiv : the preprint server for biology · 2026Article
- UCHL1 stabilizes Twist1 via K11/K63-linked deubiquitination to drive tumor metastasis in non-small cell lung cancer.Cell death discovery · 2025Article
- TWIST1 Modulates Cilia Length, Endocytic Vesicle Dynamics, and Cell-Cell Junctions during Neural Tube Morphogenesis.bioRxiv : the preprint server for biology · 2025Article
- RelA Inhibits Embryonic Myogenesis by Coordinately Regulating a Novel Distal Enhancer of Myogenin.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Article
- Exploring cellular changes in ruptured human quadriceps tendons at single-cell resolution.The Journal of physiology · 2025Article
- HTT loss-of-function contributes to RNA deregulation in developing Huntington's disease neurons.Cell & bioscience · 2025Article
230 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 4 institutions in 2 countries.
Funding
Abstract
This article reviews the molecular structure, expression pattern, physiological function, pathological roles and molecular mechanisms of Twist1 in development, genetic disease and cancer. Twist1 is a basic helix-loop-helix domain-containing transcription factor. It forms homo- or hetero-dimers in order to bind the Nde1 E-box element and activate or repress its target genes. During development, Twist1 is essential for mesoderm specification and differentiation. Heterozygous loss-of-function mutations of the human Twist1 gene cause several diseases including the Saethre-Chotzen syndrome. The Twist1-null mouse embryos die with unclosed cranial neural tubes and defective head mesenchyme, somites and limb buds. Twist1 is expressed in breast, liver, prostate, gastric and other types of cancers, and its expression is usually associated with invasive and metastatic cancer phenotypes. In cancer cells, Twist1 is upregulated by multiple factors including SRC-1, STAT3, MSX2, HIF-1α, integrin-linked kinase and NF-κB. Twist1 significantly enhances epithelial-mesenchymal transition (EMT) and cancer cell migration and invasion, hence promoting cancer metastasis. Twist1 promotes EMT in part by directly repressing E-cadherin expression by recruiting the nucleosome remodeling and deacetylase complex for gene repression and by upregulating Bmi1, AKT2, YB-1, etc. Emerging evidence also suggests that Twist1 plays a role in expansion and chemotherapeutic resistance of cancer stem cells. Further understanding of the mechanisms by which Twist1 promotes metastasis and identification of Twist1 functional modulators may hold promise for developing new strategies to inhibit EMT and cancer metastasis.
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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.