ArticleMolecular medicine (Cambridge, Mass.)2023
Loss of Krüppel-like factor-10 facilitates the development of chemical-induced liver cancer in mice.
Article in Molecular medicine (Cambridge, Mass.), 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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4 citing papers in PubMed, 5 citations in OpenAlex.
- Zinc finger protein-associated gene signature serves as a potential predictor for prognosis and therapeutic response in lung adenocarcinoma.Amino acids · 2026Article
- Single-cell analysis reveals KLF10-high macrophages induced by glioblastoma cells are associated with tumor progression.Frontiers in immunology · 2026Article
- Discovering the Potential Role of the C2 DUSP2+ MCs Subgroup in Lung Adenocarcinoma.Translational oncology · 2025Article
- Overexpression of ZFP69B promotes hepatocellular carcinoma growth by upregulating the expression of TLX1 and TRAPPC9.Cell division · 2024Article
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6 authors at 3 institutions in 1 country.
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Abstract
backgroundKrüppel-like factor 10 (KLF10) is involved in a positive feedback loop that regulates transforming growth factor β (TGFβ) signaling, and TGFβ plays an important role in the pathogenesis of liver disease. Here, we investigated whether KLF10 deletion affects the development of liver fibrosis and hepatocellular carcinoma (HCC).
methodsWe induced KLF10 deletion in C57BL/6 mice. Liver fibrosis was induced by feeding a diet high in fat and sucrose (high-fat diet [HFD]), whereas HCC was produced by intraperitoneal administration of N-diethylnitrosamine (DEN). An in vitro experiment was performed to evaluate the role of KLF10 in the cancer microenvironment using Hep3B and LX2 cells. An immunohistochemical study of KLF10 expression was performed using human HCC samples from 60 patients who had undergone liver resection.
resultsKLF10 deletion resulted in an increased DEN-induced HCC burden with significant upregulation of SMAD2, although loss of KLF10 did not alter HFD-induced liver fibrosis. DEN-treated mice with KLF10 deletion exhibited increased levels of mesenchymal markers (N-cadherin and SNAI2) and tumor metastasis markers (matrix metalloproteinases 2 and 9). KLF10 depletion in Hep3B and LX2 cells using siRNA was associated with increased invasiveness. Compared with co-culture of KLF10-preserved Hep3B cells and KLF10-intact LX2 cells, co-culture of KLF10-preserved Hep3B cells and KLF10-depleted LX2 cells resulted in significantly enhanced invasion. Low KLF10 expression in resected human HCC specimens was associated with poor survival.
conclusionThe results of this study suggest that loss of KLF10 facilitates liver cancer development with alteration in TGFβ signaling.
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