Herein, we purposed to explore whether hypoxia triggers proliferation of cholesteatoma keratinocytes via the PI3K-Akt signaling cascade. Cells were inoculated with different concentration of CoCl2. The proliferation and cellular HIF-1α, p-PDK1 and p‑Akt expression levels of cholesteatoma keratinocytes were assessed in vitro. Hypoxia escalated cell proliferation via upregulating p-PDK1 and p‑Akt expressions. Specific inhibitor of the PI3K-Akt signaling cascade, LY294002 markedly inhibited the expression of p‑Akt and significantly reduces the hypoxia‑induced proliferation of cholesteatoma keratinocytes. Our data provides research evidence confirming that hypoxia participates in the onset and progress of cholesteatoma.

中文翻译：

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氯化钴刺激的缺氧通过 PI3K/Akt 信号通路促进胆脂瘤角质形成细胞的增殖。

在此，我们旨在探索缺氧是否通过 PI3K-Akt 信号级联触发胆脂瘤角质形成细胞的增殖。用不同浓度的 CoCl2 接种细胞。在体外评估胆脂瘤角质形成细胞的增殖和细胞 HIF-1α、p-PDK1 和 p-Akt 表达水平。缺氧通过上调 p-PDK1 和 p-Akt 表达促进细胞增殖。PI3K-Akt 信号级联的特异性抑制剂 LY294002 显着抑制 p-Akt 的表达，并显着降低缺氧诱导的胆脂瘤角质形成细胞增殖。我们的数据提供了研究证据，证实缺氧参与了胆脂瘤的发病和进展。