ArticleScientific reports2025
NFATc1 facilitates hepatocellular carcinoma progression by regulating the senescence-associated secretory phenotype.
Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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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.
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
6 citing papers in PubMed.
- Intracellular Calcium Overload Promotes NFATc1-ATF3 Activation and Induces the Senescence-Associated Phenotype in Irradiated Osteocytes.Life (Basel, Switzerland) · 2026Article
- Integration of bulk and single-cell RNA-seq data identifies a cellular senescence-related prognostic signature in liver hepatocellular carcinoma.Discover oncology · 2026Article
- Stem Cells in Aging and Anti-Aging.Stem cell reviews and reports · 2026Review
- Energy Metabolism and Cancer Pain: A Pathway to Innovative Treatment Strategies.Current topics in medicinal chemistry · 2026Review
- Therapy-Induced Senescence (TIS) and SASP: The p53-Mediated Interplay in Cancer Progression and Treatment.International journal of molecular sciences · 2025Review
- Single Nucleus MultiOmics Links Novel Transcription Factor Motifs to Murine Hepatic Sex Differences in Chromatin Accessibility and Metabolic Dysfunction-Associated Steatotic Liver Disease.bioRxiv : the preprint server for biology · 2025Article
Corrections and comments
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Authors and funding
8 authors.
Funding
Abstract
The Nuclear Factor of Activated T-cells cytoplasmic 1 (NFATc1) is identified to be an oncogene in several human cancers. However, its specific role in HCC progression and the relevant mechanisms remain unclear. To investigate this, we analyzed NFATc1 expression in clinical HCC samples (n = 289) using RT-qPCR, Western blotting, and immunohistochemistry (IHC). In vitro assays assessed HCC cell proliferation, migration, invasion, apoptosis, and cell cycle, while in vivo studies using BALB/c nude mice evaluated the effects of NFATc1 on HCC growth and metastasis. Mechanistic studies were conducted to explore NFATc1's downstream signaling pathways. Results revealed that NFATc1 is significantly upregulated in HCC tissues compared to adjacent non-cancerous tissues, correlating with poor prognosis. Overexpression of NFATc1 enhanced HCC cell proliferation, migration, and invasion both in vitro and in vivo, while silencing NFATc1 reduced these malignant traits. Mechanistic analysis indicated that NFATc1 activation correlates with NF-κB/TMP21 signaling and senescence-associated secretory phenotype (SASP) amplification, independent of growth arrest. These findings suggest that NFATc1 plays a pivotal role in HCC progression, potentially through the modulation of SASP activation. Targeting NFATc1 and its signaling pathways could be a promising therapeutic approach for HCC.
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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.