ArticleFrontiers in oncology2020
NFATc Acts as a Non-Canonical Phenotypic Stability Factor for a Hybrid Epithelial/Mesenchymal Phenotype.
Article in Frontiers in oncology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers, 1 of them a synthesis that pooled it.
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Who cites it
27 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Endothelial-to-mesenchymal transition and vasculogenic mimicry in tumor vascular plasticity: a comparative bibliometric analysis and mechanistic framework.Frontiers in oncology · 2026Pooled it
- Systems-level analysis identifies IRF6 as an inhibitor of epithelial-mesenchymal transition.Journal of biological engineering · 2026Article
- Identification, functional insights and therapeutic targeting of EMT tumour states.Nature reviews. Cancer · 2026Review
- Connexin43 functions as a non-canonical phenotypic stability factor in promoting hybrid Epithelial/Mesenchymal phenotype in glioblastoma cells.Translational oncology · 2025Article
- An integrative phenotype-structured partial differential equation model for the population dynamics of epithelial-mesenchymal transition.NPJ systems biology and applications · 2025Article
- Article
- Endosomal pH is an evolutionarily conserved driver of phenotypic plasticity in colorectal cancer.NPJ systems biology and applications · 2024Article
- Phenotypic Plasticity and Cancer: A System Biology Perspective.Journal of clinical medicine · 2024Review
- Leveraging Cancer Phenotypic Plasticity for Novel Treatment Strategies.Journal of clinical medicine · 2024Article
- How important is EMT for cancer metastasis?PLoS biology · 2024Article
- The epithelial-mesenchymal plasticity landscape: principles of design and mechanisms of regulation.Nature reviews. Genetics · 2023Review
- Spatial transcriptomics reveals distinct and conserved tumor core and edge architectures that predict survival and targeted therapy response.Nature communications · 2023Article
- Population dynamics of EMT elucidates the timing and distribution of phenotypic intra-tumoral heterogeneity.iScience · 2023Article
- Network topology metrics explaining enrichment of hybrid epithelial/mesenchymal phenotypes in metastasis.PLoS computational biology · 2022Article
- P4HA2: A link between tumor-intrinsic hypoxia, partial EMT and collective migration.Advances in cancer biology - metastasis · 2022Article
- Interconnected high-dimensional landscapes of epithelial-mesenchymal plasticity and stemness in cancer.Clinical & experimental metastasis · 2022Review
- Transcriptional and post-transcriptional control of epithelial-mesenchymal plasticity: why so many regulators?Cellular and molecular life sciences : CMLS · 2022Review
- Review
- Mean residence times of TF-TF and TF-miRNA toggle switches.Journal of biosciences · 2022Article
- Mapping phenotypic heterogeneity in melanoma onto the epithelial-hybrid-mesenchymal axis.Frontiers in oncology · 2022Article
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Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Metastasis remains the cause of over 90% of cancer-related deaths. Cells undergoing metastasis use phenotypic plasticity to adapt to their changing environmental conditions and avoid therapy and immune response. Reversible transitions between epithelial and mesenchymal phenotypes - epithelial-mesenchymal transition (EMT) and its reverse mesenchymal-epithelial transition (MET) - form a key axis of phenotypic plasticity during metastasis and therapy resistance. Recent studies have shown that the cells undergoing EMT/MET can attain one or more hybrid epithelial/mesenchymal (E/M) phenotypes, the process of which is termed as partial EMT/MET. Cells in hybrid E/M phenotype(s) can be more aggressive than those in either epithelial or mesenchymal state. Thus, it is crucial to identify the factors and regulatory networks enabling such hybrid E/M phenotypes. Here, employing an integrated computational-experimental approach, we show that the transcription factor nuclear factor of activated T-cell (NFATc) can inhibit the process of complete EMT, thus stabilizing the hybrid E/M phenotype. It increases the range of parameters enabling the existence of a hybrid E/M phenotype, thus behaving as a phenotypic stability factor (PSF). However, unlike previously identified PSFs, it does not increase the mean residence time of the cells in hybrid E/M phenotypes, as shown by stochastic simulations; rather it enables the co-existence of epithelial, mesenchymal and hybrid E/M phenotypes and transitions among them. Clinical data suggests the effect of NFATc on patient survival in a tissue-specific or context-dependent manner. Together, our results indicate that NFATc behaves as a non-canonical PSF for a hybrid E/M phenotype.
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