Leukemia Inhibitory Factor via JAK‐STAT Signaling Drives Beryllium Sulfate–Induced Epithelial–Mesenchymal Transition in 16HBE Cells DOI
Yaqi Li,

Zhanbing Sun,

Yuqi Tong

et al.

Journal of Applied Toxicology, Journal Year: 2025, Volume and Issue: unknown

Published: May 1, 2025

Beryllium and its compounds are classified as carcinogens, prolonged exposure can trigger chronic beryllium disease. The Janus kinase-signal transducer activator of transcription (JAK-STAT) signaling is known to play a critical role in the development progression numerous diseases. Leukemia inhibitory factor (LIF), key upstream cytokine JAK-STAT pathway, has been implicated regulating inflammatory responses epithelial-mesenchymal transition (EMT) various However, specific involvement pathway LIF sulfate (BeSO₄)-induced EMT human bronchial epithelial (16HBE) cells remains unclear. To investigate regulatory mechanisms, we examined effects BeSO₄ on 16HBE targeted using both pharmacological inhibition (niclosamide) genetic silencing LIF. Subsequently, assessed cell morphology, proliferative capacity, protein levels, marker expression. Our findings demonstrated that inhibited proliferation activated pathway. Pretreatment with niclosamide significantly mitigated cellular inflammation process induced by BeSO₄. Additionally, markedly reduced activation decreased expression markers. This study uncovers novel mechanism underlying BeSO₄-induced cells, providing valuable insights into molecular mechanisms toxicity compounds.

Language: Английский

Leukemia Inhibitory Factor via JAK‐STAT Signaling Drives Beryllium Sulfate–Induced Epithelial–Mesenchymal Transition in 16HBE Cells DOI
Yaqi Li,

Zhanbing Sun,

Yuqi Tong

et al.

Journal of Applied Toxicology, Journal Year: 2025, Volume and Issue: unknown

Published: May 1, 2025

Beryllium and its compounds are classified as carcinogens, prolonged exposure can trigger chronic beryllium disease. The Janus kinase-signal transducer activator of transcription (JAK-STAT) signaling is known to play a critical role in the development progression numerous diseases. Leukemia inhibitory factor (LIF), key upstream cytokine JAK-STAT pathway, has been implicated regulating inflammatory responses epithelial-mesenchymal transition (EMT) various However, specific involvement pathway LIF sulfate (BeSO₄)-induced EMT human bronchial epithelial (16HBE) cells remains unclear. To investigate regulatory mechanisms, we examined effects BeSO₄ on 16HBE targeted using both pharmacological inhibition (niclosamide) genetic silencing LIF. Subsequently, assessed cell morphology, proliferative capacity, protein levels, marker expression. Our findings demonstrated that inhibited proliferation activated pathway. Pretreatment with niclosamide significantly mitigated cellular inflammation process induced by BeSO₄. Additionally, markedly reduced activation decreased expression markers. This study uncovers novel mechanism underlying BeSO₄-induced cells, providing valuable insights into molecular mechanisms toxicity compounds.

Language: Английский

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