ArticleNature cancer2024
Two distinct epithelial-to-mesenchymal transition programs control invasion and inflammation in segregated tumor cell populations.
Article in Nature cancer, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 71 papers.
What it found
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Who cites it
71 citing papers in PubMed.
- Decoding epithelial-mesenchymal transitions with multi-omics.Nature reviews. Genetics · 2026Review
- In silico discovery of natural and synthetic inhibitors targeting AKT1 in prostate cancer.Molecular diversity · 2026Article
- NHSL3 knockout modulates sorafenib response, growth, and motility in hepatocellular carcinoma cell models.Molecular biology reports · 2026Article
- Spatial transcriptomics reveals atorvastatin modulates the tumor microenvironment to suppress breast cancer liver metastatic outgrowth.Neoplasia (New York, N.Y.) · 2026Article
- Epithelial-mesenchymal transition in carcinoma: navigating phenotypic states to target resistance and metastasis.Cancer metastasis reviews · 2026Review
- Intrinsic cellular heterogeneity directs divergent epithelial-to-mesenchymal transition outcomes.The FEBS journal · 2026Article
- CD47 promotes mitogen-activated protein kinase and epithelial-to-mesenchymal transition molecular programs to drive prometastatic phenotypes in non-small cell lung cancer.Molecular oncology · 2026Article
- CYP4B1 inhibits lung adenocarcinoma metastasis by downregulating slug transcription via Sp1.Clinical & experimental metastasis · 2026Article
- DICER1-related tumour predisposition mutations increase 3p-miRNA function and HERVH activity.Nature communications · 2026Article
- Review
- Multiple distinct metastatic cell states are induced by epithelial-mesenchymal plasticity.bioRxiv : the preprint server for biology · 2026Article
- Single-cell multimodal profiling of pan-cancer cell lines uncovers gene regulatory principles underlying intrinsic cell states and environmental features.Nature communications · 2026Article
- Neural crest cell signatures drive tumorigenesis in tuberous sclerosis complex and lymphangioleiomyomatosis.JCI insight · 2026Article
- Systems-Level Mapping of the Tumor Microenvironment Reveals Immune-Mediated Mechanisms and Potential Targets in Platinum-Resistant Ovarian Cancer.Research square · 2026Article
- Chalcones as multitarget modulators in non-small cell lung cancer: mechanistic insights and therapeutic perspectives.Archives of toxicology · 2026Review
- Tumor heterogeneity: development, mechanisms, and therapeutic implications.Signal transduction and targeted therapy · 2026Review
- CDH2 marks a fibroblast-associated stromal cell state in pancreatic ductal adenocarcinoma.Human cell · 2026Article
- Single cell multiomics unravel the transcription networks controlling the different EMT tumor states.Nature communications · 2026Article
- Cancer stem cell plasticity: mechanisms, immune microenvironment crosstalk, and therapeutic implications.Journal of hematology & oncology · 2026Review
- Interpretable and scalable spatial gene set activity analysis with GESSO uncovers functional tissue architecture.bioRxiv : the preprint server for biology · 2026Article
11 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
13 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Epithelial-to-mesenchymal transition (EMT) triggers cell plasticity in embryonic development, adult injured tissues and cancer. Combining the analysis of EMT in cell lines, embryonic neural crest and mouse models of renal fibrosis and breast cancer, we find that there is not a cancer-specific EMT program. Instead, cancer cells dedifferentiate and bifurcate into two distinct and segregated cellular trajectories after activating either embryonic-like or adult-like EMTs to drive dissemination or inflammation, respectively. We show that SNAIL1 acts as a pioneer factor in both EMT trajectories, and PRRX1 drives the progression of the embryonic-like invasive trajectory. We also find that the two trajectories are plastic and interdependent, as the abrogation of the EMT invasive trajectory by deleting Prrx1 not only prevents metastasis but also enhances inflammation, increasing the recruitment of antitumor macrophages. Our data unveil an additional role for EMT in orchestrating intratumor heterogeneity, driving the distribution of functions associated with either inflammation or metastatic dissemination.
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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.