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- W4379617764 abstract "Hypoxia inducible factor-1ɑ (HIF-1ɑ) is the regulatory subunit of the HIF-1 transcription factor that is a regulator of cell physiological responses to hypoxia. However, the biological function and regulatory mechanisms controlling HIF-1α in normoxia are poorly understood. Here, we first examined the role of HIF-1α in the inflammatory activation of A549 human lung carcinoma cells in normoxia. Inactivation of the HIF-1α gene by CRISPR/Cas9 reduced the secretion of CXCL8 induced by stimulation with a cytokine mixture (CM) consisting of IL-1, TNFα and IFNγ. We next determined that cytokines act co-operatively to induce expression and nuclear accumulation of HIF-1α. To investigate the signalling mechanisms by which cytokines induce HIF-1α in normoxia, pharmacological inhibitors against the Jak/STAT, PI3K, NFκB, MEK/ERK, and JNK pathways were used. Inhibition of the Jak/STAT and JNK pathways inhibited the induction and nuclear accumulation of HIF-1ɑ by cytokines. Furthermore, siRNA knockdown of STAT1 and JNK also reduced the induction of HIF-1α by cytokines. Finally, pharmacological inhibition of these two pathways also blocked the trans-activation of HIF-1. These findings have implications for understanding the role and regulatory mechanisms of HIF-1ɑ in inflammation and cell biology." @default.
- W4379617764 created "2023-06-08" @default.
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- W4379617764 date "2023-08-01" @default.
- W4379617764 modified "2023-09-26" @default.
- W4379617764 title "Cytokine induction of HIF-1α during normoxia in A549 human lung carcinoma cells is regulated by STAT1 and JNK signalling pathways" @default.
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- W4379617764 doi "https://doi.org/10.1016/j.molimm.2023.06.001" @default.
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