ArticleJournal of clinical and translational hepatology2022
KRT17 Promotes the Activation of HSCs via EMT in Liver Fibrosis.
Article in Journal of clinical and translational hepatology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 15 citations in OpenAlex.
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- Nurr1 attenuates hepatic stellate cell activation by inhibiting EMT and cell cycle progression via interaction with Smad3.Molecular biology reports · 2025Article
- Epithelial Cell Dysfunction in Pulmonary Fibrosis: Mechanisms, Interactions, and Emerging Therapeutic Targets.Pharmaceuticals (Basel, Switzerland) · 2025Review
- HIF-1α/LTBP2 axis activate HSCs to promote liver fibrosis by interacting with LOXL1 via the ERK pathway.Cellular and molecular life sciences : CMLS · 2025Article
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- Decoding the Tumor Microenvironment of Myoepithelial Cells in Triple-Negative Breast Cancer Through Single-Cell and Transcriptomic Sequencing and Establishing a Prognostic Model Based on Key Myoepithelial Cell Genes.International journal of genomics · 2025Article
- Oxidative Stress and Annexin A2 Differential Expression in Free Fatty Acids-Induced Non-Alcoholic Fatty Liver Disease in HepG2 Cells.International journal of molecular sciences · 2024Article
- CHEK2 knockout is a therapeutic target for TP53-mutated hepatocellular carcinoma.Cell death discovery · 2024Article
- Integrated analysis reveals the molecular features of fibrosis in triple-negative breast cancer.Molecular therapy oncolytics · 2022Article
- Human liver tissue transcriptomics revealed immunometabolic disturbances and related biomarkers in hepatitis B virus-related acute-on-chronic liver failure.Frontiers in microbiology · 2022Article
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background and Aims: Although activation of hepatic stellate cells (HSCs) plays a central role in the development of liver fibrosis, the mechanism underlying the activation of HSCs remains unclear. Keratin 17 (KRT17), a member of the intermediate filament family, can regulate tumor cell proliferation and migration. The current study aimed to elucidate the role of KRT17 in the activation of HSCs and the mechanisms underlying liver fibrosis. Methods: The expression of KRT17 was determined using immunohistochemistry in tissue microarray. Western blotting and qRT-PCR assays were used to determine the KRT17 expression in fibrotic liver tissues obtained from human subjects and mice. LX-2 cells were treated with TGF-β1 recombinant protein and adipocyte differentiation mixture (MDI) mix to induce and reverse LX-2 cell activation, respectively, in order to explore the correlation between KRT17 and HSC activation. Additionally, cell proliferation and migration abilities of LX-2 cells transfected with KRT17-overexpressing plasmid or small interfering RNA were determined using CCK-8, flow cytometry, Transwell, and wound healing assays. Finally, rescue assay was used to explore the role of KRT17 in HSC activation and epithelial-mesenchymal transition (EMT). Results: The expression of KRT17 was higher in the human and mouse fibrotic liver tissues than in healthy liver tissues, and it was positively correlated with HSC activation. Upregulated KRT17 enhanced proliferation, migration, HSC activation and EMT in LX-2 cells, while knockdown of KRT17 reversed these effects. TGF-β1 recombinant protein accelerated KRT17-mediated EMT, HSC activation and proliferation, while TGF-β1 inhibitor counteracted the effect of KRT17 Conclusions: KRT17 promoted HSC activation, proliferation and EMT in hepatic fibrosis probably via TGF-β1 signaling, and KRT17 might serve as a therapeutic target for the treatment of liver fibrosis.
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