ArticleCell death & disease2022
Loss of SNAI1 induces cellular plasticity in invasive triple-negative breast cancer cells.
Article in Cell death & disease, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 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
17 citing papers in PubMed, 22 citations in OpenAlex.
- SNAI1 ablation alters integrin-mediated adhesion and endocytic fate.Cell death & disease · 2026Article
- Single-cell multimodal profiling of pan-cancer cell lines uncovers gene regulatory principles underlying intrinsic cell states and environmental features.Nature communications · 2026Article
- Single-cell multimodal profiling of pan-cancer cell lines uncovers gene regulatory principles underlying intrinsic cell states and environmental features.bioRxiv : the preprint server for biology · 2026Article
- Integrative Single-Cell and Machine Learning Analysis Identifies an EMT-Associated Prognostic Signature for Papillary Thyroid Cancer.Cancer medicine · 2026Article
- TGFβ signaling promotes cell cycle progression and resistance to the CDK4/6 inhibitor palbociclib through SOX4 transcriptional modulation in breast cancer cells.Cell death & disease · 2026Article
- Crucial Contribution of BACH1 to Bladder Cancer Progression via Upregulating Epithelial-Mesenchymal Transition Pathway.Cancer science · 2026Article
- The long noncoding RNA VIM-AS1 and nucleoporin Nup358/RanBP2 regulate SMAD nuclear accumulation during TGF-β signaling.Nucleic acids research · 2026Article
- The transcription factor LHX2 mediates and enhances oncogenic BMP signaling in medulloblastoma.Cell death and differentiation · 2025Article
- Identification of a SNAI1 enhancer RNA that drives cancer cell plasticity.Nature communications · 2025Article
- TGF-β induces cholesterol accumulation to regulate the secretion of tumor-derived extracellular vesicles.Journal of experimental & clinical cancer research : CR · 2025Article
- Transcription factors and hormone receptors: Sex‑specific targets for cancer therapy (Review).Oncology letters · 2025Review
- RAB4A is a master regulator of cancer cell stemness upstream of NUMB-NOTCH signaling.Cell death & disease · 2024Article
- Continuous exposure to doxorubicin induces stem cell-like characteristics and plasticity in MDA-MB-231 breast cancer cells identified with the SORE6 reporter.Cancer chemotherapy and pharmacology · 2024Article
- SNAI1: a key modulator of survival in lung squamous cell carcinoma and its association with metastasis.Journal of cardiothoracic surgery · 2024Article
- TFAP2A downregulation mediates tumor-suppressive effect of miR-8072 in triple-negative breast cancer via inhibiting SNAI1 transcription.Breast cancer research : BCR · 2024Article
- USP10 promotes intrahepatic cholangiocarcinoma cell survival and stemness via SNAI1 deubiquitination.Journal of molecular histology · 2023Article
- Cancer Stem Cells and Androgen Receptor Signaling: Partners in Disease Progression.International journal of molecular sciences · 2023Review
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 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The transcription factor SNAI1 mediates epithelial-mesenchymal transition, fibroblast activation and controls inter-tissue migration. High SNAI1 expression characterizes metastatic triple-negative breast carcinomas, and its knockout by CRISPR/Cas9 uncovered an epithelio-mesenchymal phenotype accompanied by reduced signaling by the cytokine TGFβ. The SNAI1 knockout cells exhibited plasticity in differentiation, drifting towards the luminal phenotype, gained stemness potential and could differentiate into acinar mammospheres in 3D culture. Loss of SNAI1 de-repressed the transcription factor FOXA1, a pioneering factor of mammary luminal progenitors. FOXA1 induced a specific gene program, including the androgen receptor (AR). Inhibiting AR via a specific antagonist regenerated the basal phenotype and blocked acinar differentiation. Thus, loss of SNAI1 in the context of triple-negative breast carcinoma cells promotes an intermediary luminal progenitor phenotype that gains differentiation plasticity based on the dual transcriptional action of FOXA1 and AR. This function of SNAI1 provides means to separate cell invasiveness from progenitor cell de-differentiation as independent cellular programs.
Indexed as
Identifiers
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.