ArticleThe EMBO journal2015
Antithetical NFATc1-Sox2 and p53-miR200 signaling networks govern pancreatic cancer cell plasticity.
Article in The EMBO journal, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers.
What it found
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Who cites it
64 citing papers in PubMed, 94 citations in OpenAlex.
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- Nuclear factor of activated T cells as a driver of tumor progression and a target for precision therapy.Animal models and experimental medicine · 2026Review
- Two Faces of NFAT Transcription Factors in LymphocytesBiomolecules · 2026Review
- MRPS16 Regulates NFATC2 Through the Wnt/β-Catenin Pathway to Promote Glioma Proliferation.Journal of cellular and molecular medicine · 2026Article
- The Multifaceted Role of p53 in Cancer Molecular Biology: Insights for Precision Diagnosis and Therapeutic Breakthroughs.Biomolecules · 2025Review
- NFATc1 facilitates hepatocellular carcinoma progression by regulating the senescence-associated secretory phenotype.Scientific reports · 2025Article
- WNT5B drives osteosarcoma stemness, chemoresistance and metastasis.Clinical and translational medicine · 2024Article
- Molecular profile of metastasis, cell plasticity and EMT in pancreatic cancer: a pre-clinical connection to aggressiveness and drug resistance.Cancer metastasis reviews · 2024Review
- Cancer cell plasticity, stem cell factors, and therapy resistance: how are they linked?Cancer metastasis reviews · 2024Review
- SOX2 Expression Does Not Guarantee Cancer Stem Cell-like Characteristics in Lung Adenocarcinoma.Cells · 2024Article
- USP7-mediated JUND suppresses RCAN2 transcription and elevates NFATC1 to enhance stem cell property in colorectal cancer.Cell biology and toxicology · 2023Article
- p53 isoform expression promotes a stemness phenotype and inhibits doxorubicin sensitivity in breast cancer.Cell death & disease · 2023Article
- Pancreatic cancer stemness: dynamic status in malignant progression.Journal of experimental & clinical cancer research : CR · 2023Review
- Breast cancer tumor microenvironment affects Treg/IL-17-producing Treg/Th17 cell axis: Molecular and therapeutic perspectives.Molecular therapy oncolytics · 2023Review
- Proliferation, apoptosis and invasion of human lung cancer cells are associated with NFATc1.Experimental and therapeutic medicine · 2023Article
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- Salt-inducible kinase 3 protects tumor cells from cytotoxic T-cell attack by promoting TNF-induced NF-κB activation.Journal for immunotherapy of cancer · 2022Article
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4 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
24 authors at 8 institutions in 3 countries.
Funding
Abstract
In adaptation to oncogenic signals, pancreatic ductal adenocarcinoma (PDAC) cells undergo epithelial-mesenchymal transition (EMT), a process combining tumor cell dedifferentiation with acquisition of stemness features. However, the mechanisms linking oncogene-induced signaling pathways with EMT and stemness remain largely elusive. Here, we uncover the inflammation-induced transcription factor NFATc1 as a central regulator of pancreatic cancer cell plasticity. In particular, we show that NFATc1 drives EMT reprogramming and maintains pancreatic cancer cells in a stem cell-like state through Sox2-dependent transcription of EMT and stemness factors. Intriguingly, NFATc1-Sox2 complex-mediated PDAC dedifferentiation and progression is opposed by antithetical p53-miR200c signaling, and inactivation of the tumor suppressor pathway is essential for tumor dedifferentiation and dissemination both in genetically engineered mouse models (GEMM) and human PDAC. Based on these findings, we propose the existence of a hierarchical signaling network regulating PDAC cell plasticity and suggest that the molecular decision between epithelial cell preservation and conversion into a dedifferentiated cancer stem cell-like phenotype depends on opposing levels of p53 and NFATc1 signaling activities.
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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 Socratic graph.