ArticleDigestive diseases and sciences2025
NFAT2 Induces Tumor Cell Proliferation and Metastasis by Acting as a Transcriptional Co-activator of the TGF-β1/SMAD Signaling Pathway and Inducing the Epithelial-Mesenchymal Transition in Liver Cancer.
Article in Digestive diseases and sciences, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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Who cites it
3 citing papers in PubMed.
- Platelets as localized conduits of TGF-β1 in the tumor microenvironment: implications for cancer progression and therapy.Human cell · 2026Review
- Spatiotemporal heterogeneity of neutrophil extracellular traps in hepatocellular carcinoma microenvironment and targeted therapy progress.Journal of translational medicine · 2026Review
- Revolutionizing cervical cancer treatment: single-cell sequencing ofFrontiers in immunology · 2025Article
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Authors and funding
9 authors.
Funding
Abstract
backgroundThe role of NFAT2 in liver cancer is conflicting, with evidence suggesting both oncogenic and tumor-suppressive effects. A clear understanding of its expression, function, regulation, and mechanism of action in liver cancer remains critical.
objectivesTo examine the expression levels, biological functions, regulatory mechanisms, and downstream pathways of NFAT2 in liver cancer and its metastasis.
methodsThe expression of NFAT2 was analyzed in liver cancer patients and correlated with clinical outcomes. Functional assays, including proliferation, migration, invasion, and xenograft models, were employed to assess the effects of NFAT2 upregulation and downregulation. Molecular analyses were conducted to identify key pathways and protein interactions underpinning NFAT2's effects. The therapeutic potential of NFAT2 inhibition in combination with sorafenib was also evaluated.
resultsNFAT2 overexpression was associated with poor prognosis and shorter disease-free survival in liver cancer patients. Upregulation of NFAT2 promoted hepatoma cell proliferation, migration, and invasion, while its downregulation impaired these pro-oncogenic effects. Mechanistically, NFAT2 enhanced the epithelial-to-mesenchymal transition (EMT) by increasing mesenchymal marker expression (N-cadherin, vimentin, MMP9) and decreasing invasion inhibitors (E-cadherin, ZO-1). It physically interacted with SMAD3 and p300, thereby activating the TGF-β1/SMAD pathway to drive tumor progression. NFAT2 knockdown or inhibition re-sensitized tumor cells to sorafenib, indicating its promising therapeutic potential.
conclusionNFAT2 acts as a transcriptional co-activator of the TGF-β1/SMAD signaling pathway, promoting liver cancer progression and metastasis. Its inhibition could serve as a novel therapeutic strategy for the treatment of advanced liver cancer, particularly in combination with sorafenib.
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40038210What Socratic 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 Socratic graph.