ArticleMolecular cancer research : MCR2011
Temporal and spatial cooperation of Snail1 and Twist1 during epithelial-mesenchymal transition predicts for human breast cancer recurrence.
Article in Molecular cancer research : MCR, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 104 papers.
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Who cites it
104 citing papers in PubMed, 224 citations in OpenAlex.
- PRAME promotes invasion and metastasis of salivary adenoid cystic carcinoma by regulating RARα stability via the cullin2 ubiquitin-proteasome system.Clinical and translational medicine · 2026Article
- Partial EMT Drives Persistent Collective Migration via Collision Guidance in Heterogeneous Populations.bioRxiv : the preprint server for biology · 2026Article
- Mesenchymal to epithelial transition (MET) in cancer progression: insights from logical modeling.Scientific reports · 2026Article
- STAT3 axis in cancer and cancer stem cells: From oncogenesis to targeted therapies.Biochimica et biophysica acta. Reviews on cancer · 2025Review
- AXL-TBK1 driven AKT3 activation promotes metastasis.Science signaling · 2024Article
- Characteristics and transcriptional regulators of spontaneous epithelial-mesenchymal transition in genetically unperturbed patient-derived non-spindled breast carcinoma.Breast cancer research : BCR · 2024Article
- Normalization of Snai1-mediated vessel dysfunction increases drug response in cancer.Oncogene · 2024Article
- Exploring the Function of Epicardial Cells Beyond the Surface.Circulation research · 2024Review
- Dissecting the multifaceted roles of autophagy in cancer initiation, growth, and metastasis: from molecular mechanisms to therapeutic applications.Medical oncology (Northwood, London, England) · 2024Review
- TRPA1 Contributes to FGFR2c Signaling and to Its Oncogenic Outcomes in Pancreatic Ductal Adenocarcinoma-Derived Cell Lines.Cancers · 2024Article
- Modulation of Autophagy Direction to Enhance Antitumor Effect of Endoplasmic-Reticulum-Targeted Therapy: Left or Right?Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023Article
- Article
- Molecular mechanisms and therapeutic applications of huaier in breast cancer treatment.Frontiers in pharmacology · 2023Review
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- Epithelial-mesenchymal transition: The history, regulatory mechanism, and cancer therapeutic opportunities.MedComm · 2022Review
- Epicardium-derived cells organize through tight junctions to replenish cardiac muscle in salamanders.Nature cell biology · 2022Article
- Autophagy-mediated degradation of NOTCH1 intracellular domain controls the epithelial to mesenchymal transition and cancer metastasis.Cell & bioscience · 2022Article
- Epithelial-mesenchymal transition and its transcription factors.Bioscience reports · 2022Review
- Snail induces dormancy in disseminated luminal type A breast cancer through Src inhibition.American journal of cancer research · 2022Article
- AXL Inhibitor TP-0903 Reduces Metastasis and Therapy Resistance in Pancreatic Cancer.Molecular cancer therapeutics · 2022Article
44 more citing papers are in PubMed but not listed here.
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Epithelial-mesenchymal transition (EMT) is a normal developmental program that is considered to also play an important role in cancer metastasis. Ultimate inducers of EMT are transcriptional repressors that individually can induce experimental EMT, yet in many cells, particularly cancer cells, multiple inducers are expressed simultaneously. Why, and if, and how they interact to regulate EMT is unanswered. Using RNA interference technology to affect protein knockdown and avoid potential overexpression artifact coupled with transient TGFβ treatment to better mimic in vivo conditions we show, in both nontumorigenic and tumorigenic epithelial cancer cells, that Snail1 is uniquely required for EMT initiation, whereas Twist1 is required to maintain late EMT. Twist1, present in resting epithelial cells, is dispensable for EMT initiation. Mechanistically, in response to transient TGFβ treatment, transient Snail1 expression represses Twist1 transcription directly, which is subsequently upregulated, as Snail1 levels decrease, to sustain E-cadherin downregulation and growth arrest of EMT. Persistent Twist1 expression is associated with a p38 and extracellular signal-regulated kinase signal feedback loop that sustains growth-inhibitory signals characteristic of quiescent micrometastatic tumors. This Snail1-Twist1 temporal and spatial cooperation was also observed in vivo during human breast cancer progression to metastasis. Twist1 level, but not Snail1 level, and Twist1:Snail1 ratio in disseminated micrometastatic bone marrow tumor cells was found to correlate with survival and treatment resistance and is highly predictive of metastatic or recurrent disease.
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