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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 CoCl(2). The proliferation and cellular HIF-1α, p-PDK1 and p‑Akt expression levels of cholesteatoma keratinoc...

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Detalles Bibliográficos
Autores principales: Zhang, Chen, Chen, Min, Tao, Qi, Chi, Zhangcai
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Ivyspring International Publisher 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8436096/
https://www.ncbi.nlm.nih.gov/pubmed/34522167
http://dx.doi.org/10.7150/ijms.60617
Descripción
Sumario: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 CoCl(2). 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.