ArticleMolecular biology reports2025
Transforming growth factor-β1 triggers the proliferation of human cholangiocyte spheroids via interleukin-6-mediated STAT3 signaling.
Article in Molecular biology reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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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.
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Who cites it
1 citing paper in PubMed.
- Bazedoxifene Attenuates Isoproterenol-Induced Cardiac Fibroblast Activation and Fibrotic Phenotype via Modulation of the IL-6/STAT3 Signaling Axis.Current issues in molecular biology · 2026Article
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Authors and funding
4 authors.
Funding
Abstract
backgroundInflammatory cytokines are crucial for various cellular mechanisms, including differentiation, fibrosis, and proliferation. Cytokine dysregulation provokes pathophysiologic conditions in cholangiocytes, even cholangiocarcinogenesis. Specifically, transforming growth factor-beta (TGF-β) and interleukin-6 (IL-6) are known to be related to cholangiocarcinoma progression. We investigated the pathophysiological signaling in normal cholangiocyte (H69) spheroids mediated by TGF-β1 or/and IL-6. METHODS AND
resultsThe spheroids were treated with TGF-β1 or/and IL-6 for 1 and 3 days, and then the secretion levels of TGF-β1 and IL-6, as well as their mediated protein expression levels, were measured. TGF-β1-mediated IL-6 signaling was assessed using TGF-β1- and IL-6-specific small interfering RNA (siRNA). The secretion of IL-6 and the expression of its receptor were significantly increased in all treated spheroids at 3 days. Treatment of spheroids with TGF-β1 or TGF-β1 plus IL-6 increased the expression of epithelial-mesenchymal transition (EMT)- and fibrosis-related proteins, but IL-6 treatment alone did not. Moreover, all treated spheroids showed a marked increase in size and the expression levels of proliferation-related proteins. Furthermore, the levels of IL-6 secretion and proliferation-related protein expression remained unchanged in TGF-β1 or/and IL-6 siRNA transfectants compared with those of the scrambled siRNA transfectant.
conclusionsOur findings suggest that long-term exposure to TGF-β1 triggers the malignant transformation of cholangiocytes by activating EMT and fibrosis, as well as IL-6/STAT3-mediated proliferation signaling.
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Registered trials
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