ArticleFrontiers in cell and developmental biology2020
Defects in mTORC1 Network and mTORC1-STAT3 Pathway Crosstalk Contributes to Non-inflammatory Hepatocellular Carcinoma.
Article in Frontiers in cell and developmental biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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Who cites it
7 citing papers in PubMed, 11 citations in OpenAlex.
- The Small Molecule H89 Facilitates Mesenchymal Stem Cell-derived Extracellular Vesicle Release and Optimizes Therapeutic Efficacy in Liver Regeneration.Journal of extracellular vesicles · 2026Article
- Folliculin depletion results in liver cell damage and cholangiocarcinoma through MiT/TFE activation.Cell death and differentiation · 2025Article
- mTORC1 and STAT3 signaling are indispensable for in vitro TGFβ1-dependent three-dimensional (3D) tendon constructs.BMB reports · 2025Article
- The Complexity and Significance of Fibroblast Growth Factor (FGF) Signaling for FGF-Targeted Cancer Therapies.Cancers · 2024Review
- Zebrafish Mutant Lines Reveal the Interplay betweenInternational journal of molecular sciences · 2022Article
- Non-cirrhotic hepatocellular carcinoma in chronic viral hepatitis: Current insights and advancements.World journal of gastroenterology · 2021Review
- FGF/FGFR Signaling in Hepatocellular Carcinoma: From Carcinogenesis to Recent Therapeutic Intervention.Cancers · 2021Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BACKGROUND AND
aimsMammalian target of rapamycin complex 1 (mTORC1) is frequently hyperactivated in hepatocellular carcinoma (HCC). Cases of HCC without inflammation and cirrhosis are not rarely seen in clinics. However, the molecular basis of non-inflammatory HCC remains unclear.
methodsSpontaneous non-inflammatory HCC in mice was triggered by constitutive elevation of mTORC1 by liver-specific
resultsWe showed that
conclusionOur findings reveal the mechanisms of mTORC1-driven non-inflammatory HCC and provide insight into further development of a protective strategy against non-inflammatory HCC.
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Registered trials
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