ArticleNPJ systems biology and applications2019
Combinatorial perturbation analysis reveals divergent regulations of mesenchymal genes during epithelial-to-mesenchymal transition.
Article in NPJ systems biology and applications, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 38 papers, 1 of them a synthesis that pooled it.
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
38 citing papers in PubMed, 1 synthesis or guideline pooled it, 64 citations in OpenAlex.
- PD-L1 Activity Is Associated with Partial EMT and Metabolic Reprogramming in Carcinomas.Current oncology (Toronto, Ont.) · 2022Pooled it
- Genetic Convergence Analysis of CRISPR Perturbations Deciphers Gene Functional Similarity.bioRxiv : the preprint server for biology · 2025Article
- Review
- Regulation of divergent epithelial-to-mesenchymal transition responses via the CDK4/6-USP51 pathway through ZEB1 protein stabilization.Scientific reports · 2025Article
- Intercellular signaling reinforces single-cell level phenotypic transitions and facilitates robust re-equilibrium of heterogeneous cancer cell populations.Cell communication and signaling : CCS · 2025Article
- Data- and theory-driven approaches for understanding paths of epithelial-mesenchymal transition.Genesis (New York, N.Y. : 2000) · 2024Review
- Population dynamics of EMT elucidates the timing and distribution of phenotypic intra-tumoral heterogeneity.iScience · 2023Article
- Dynamics of Epithelial-Mesenchymal Plasticity: What Have Single-Cell Investigations Elucidated So Far?ACS omega · 2023Review
- Involvement of Epithelial-Mesenchymal Transition Genes in Small Cell Lung Cancer Phenotypic Plasticity.Cancers · 2023Article
- Epigenetic memory acquired during long-term EMT induction governs the recovery to the epithelial state.Journal of the Royal Society, Interface · 2023Article
- Network motifs and hypermotifs in TGFβ-induced epithelial to mesenchymal transition and metastasis.Frontiers in systems biology · 2023Article
- Identification of a core EMT signature that separates basal-like breast cancers into partial- and post-EMT subtypes.Frontiers in oncology · 2023Article
- The role of tumor microenvironment in drug resistance: emerging technologies to unravel breast cancer heterogeneity.Frontiers in oncology · 2023Review
- Network topology metrics explaining enrichment of hybrid epithelial/mesenchymal phenotypes in metastasis.PLoS computational biology · 2022Article
- Article
- Robustness in phenotypic plasticity and heterogeneity patterns enabled by EMT networks.Biophysical journal · 2022Article
- Comparative single-cell transcriptomes of dose and time dependent epithelial-mesenchymal spectrums.NAR genomics and bioinformatics · 2022Article
- Population Dynamics of Epithelial-Mesenchymal Heterogeneity in Cancer Cells.Biomolecules · 2022Article
- SkewC: Identifying cells with skewed gene body coverage in single-cell RNA sequencing data.iScience · 2022Article
- Review
Corrections and comments
- Erratum issued
Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Epithelial-to-mesenchymal transition (EMT), a fundamental transdifferentiation process in development, produces diverse phenotypes in different physiological or pathological conditions. Many genes involved in EMT have been identified to date, but mechanisms contributing to the phenotypic diversity and those governing the coupling between the dynamics of epithelial (E) genes and that of the mesenchymal (M) genes are unclear. In this study, we employed combinatorial perturbations to mammary epithelial cells to induce a series of EMT phenotypes by manipulating two essential EMT-inducing elements, namely TGF-β and ZEB1. By measuring transcriptional changes in more than 700 E-genes and M-genes, we discovered that the M-genes exhibit a significant diversity in their dependency to these regulatory elements and identified three groups of M-genes that are controlled by different regulatory circuits. Notably, functional differences were detected among the M-gene clusters in motility regulation and in survival of breast cancer patients. We computationally predicted and experimentally confirmed that the reciprocity and reversibility of EMT are jointly regulated by ZEB1. Our integrative analysis reveals the key roles of ZEB1 in coordinating the dynamics of a large number of genes during EMT, and it provides new insights into the mechanisms for the diversity of EMT phenotypes.
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.