Cobalt chloride-stimulated hypoxia promotes the proliferation of cholesteatoma keratinocytes via the PI3K/Akt signaling pathway

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-1 alpha, 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.

Automated summary

Hypoxia induces proliferation of cholesteatoma keratinocytes through upregulating p-PDK1 and p-Akt expressions via the PI3K-Akt signaling cascade. Inhibition of p-Akt expression by specific inhibitor LY294002 significantly reduces hypoxia-induced cell proliferation in cholesteatoma keratinocytes. This study provides evidence supporting the involvement of hypoxia in cholesteatoma initiation and progression.