Int J Med Sci 2021; 18(15):3403-3411. doi:10.7150/ijms.60617 This issue

Research Paper

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

Chen Zhang1#, Min Chen1,2#, Qi Tao3, Zhangcai Chi1,2✉

1. Department of Otolaryngology, Eye & ENT Hospital, Fudan University, 83 Fenyang Road, Shanghai, China.
2. NHC Key Laboratory of Hearing Medicine (Fudan University), Shanghai, 200031, PR China.
3. Nursing Department, Eye & ENT Hospital, Fudan University, 83 Fenyang Road, Shanghai, China.
# Co-first authors

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Citation:
Zhang C, Chen M, Tao Q, Chi Z. Cobalt chloride-stimulated hypoxia promotes the proliferation of cholesteatoma keratinocytes via the PI3K/Akt signaling pathway. Int J Med Sci 2021; 18(15):3403-3411. doi:10.7150/ijms.60617. Available from https://www.medsci.org/v18p3403.htm

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Abstract

Graphic abstract

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.

Keywords: hypoxia, cholesteatoma, HIF-1α, cell proliferation, PI3K/Akt signaling pathway