ArticleJCI insight2020
NFATC4 promotes quiescence and chemotherapy resistance in ovarian cancer.
Article in JCI insight, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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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.
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Who cites it
36 citing papers in PubMed, 51 citations in OpenAlex.
- Targeting HDAC and proteostasis to eradicate quiescent cancer cells.Cancer gene therapy · 2026Article
- Integrative single-cell and spatial transcriptomic analysis reveals a lactate-driven crosstalk between NFATc4⁺ tumor cells and SPP1⁺ macrophages in glioblastoma.Journal of translational medicine · 2026Article
- Identification of the MRTFA/SRF pathway as a critical regulator of quiescence and chemotherapy resistance in cancer.Cancer letters · 2026Article
- The Role of Neuritin 1 in Synaptic Plasticity and Sensory Nerve Function: Integrator of Neurotrophic, Metabolic and Injury Signals.The European journal of neuroscience · 2026Review
- Mitochondrial Long Non-Coding RNAs in Gynecological Cancers: Pathogenic Signaling Pathways and Therapeutic Opportunities.Current issues in molecular biology · 2026Review
- Interplay between Epigenetic and Transcription Factors Mediating Drug Resistance via Stem Cells in Breast Cancer.ACS omega · 2025Review
- NFATc4 Promotes Lung Adenocarcinoma Progression via the CCNB1/CDK1 Pathway and Is a Potential Prognostic Biomarker.Cancer science · 2025Article
- Role of the NuRD complex and altered proteostasis in cancer cell quiescence.bioRxiv : the preprint server for biology · 2025Article
- Nuclear Factor of Activated T Cells (NFAT) Proteins as Targeted Molecules in Diseases: A Narrative Review.Cureus · 2024Review
- Acetate drives ovarian cancer quiescence via ACSS2-mediated acetyl-CoA production.Molecular metabolism · 2024Article
- Application of single cell sequencing technology in ovarian cancer research (review).Functional & integrative genomics · 2024Review
- Acetate drives ovarian cancer quiescence via ACSS2-mediated acetyl-CoA production.bioRxiv : the preprint server for biology · 2024Article
- mTOR pathway occupies a central role in the emergence of latent cancer cells.Cell death & disease · 2024Review
- Causal effect analysis of estrogen receptor associated breast cancer and clear cell ovarian cancer.American journal of translational research · 2024Article
- Decoding key cell sub-populations and molecular alterations in glioblastoma at recurrence by single-cell analysis.Acta neuropathologica communications · 2023Article
- Article
- Quiescent Ovarian Cancer Cells Secrete Follistatin to Induce Chemotherapy Resistance in Surrounding Cells in Response to Chemotherapy.Clinical cancer research : an official journal of the American Association for Cancer Research · 2023Article
- Polyploid/Multinucleated Giant and Slow-Cycling Cancer Cell Enrichment in Response to X-ray Irradiation of Human Glioblastoma Multiforme Cells Differing in Radioresistance and TP53/PTEN Status.International journal of molecular sciences · 2023Article
- Emerging roles of endoplasmic reticulum stress in the cellular plasticity of cancer cells.Frontiers in oncology · 2023Review
- Cell cycle exits and U-turns: Quiescence as multiple reversible forms of arrest.Faculty reviews · 2023Review
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
Abstract
Development of chemotherapy resistance is a major problem in ovarian cancer. One understudied mechanism of chemoresistance is the induction of quiescence, a reversible nonproliferative state. Unfortunately, little is known about regulators of quiescence. Here, we identify the master transcription factor nuclear factor of activated T cells cytoplasmic 4 (NFATC4) as a regulator of quiescence in ovarian cancer. NFATC4 is enriched in ovarian cancer stem-like cells and correlates with decreased proliferation and poor prognosis. Treatment of cancer cells with cisplatin resulted in NFATC4 nuclear translocation and activation of the NFATC4 pathway, while inhibition of the pathway increased chemotherapy response. Induction of NFATC4 activity resulted in a marked decrease in proliferation, G0 cell cycle arrest, and chemotherapy resistance, both in vitro and in vivo. Finally, NFATC4 drove a quiescent phenotype in part via downregulation of MYC. Together, these data identify NFATC4 as a driver of quiescence and a potential new target to combat chemoresistance in ovarian cancer.
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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 OpenQuestion graph.