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

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.

• Authors: Chen Zhang, Min Chen, Qi Tao, Zhangcai Chi
• Journal: International journal of medical sciences (Int J Med Sci) Vol. 18 Issue 15 Pg. 3403-3411 ( 2021) ISSN: 1449-1907 [Electronic] Australia
• PMID: 34522167 (Publication Type: Journal Article)
• Copyright: © The author(s).

Chemical References

• Cobalt
• Proto-Oncogene Proteins c-akt
• cobaltous chloride

Topics

• Cell Hypoxia (physiology)
• Cell Proliferation (physiology)
• Cholesteatoma (metabolism)
• Cobalt (administration & dosage)
• Humans
• Keratinocytes (metabolism)
• Phosphatidylinositol 3-Kinases (metabolism)
• Proto-Oncogene Proteins c-akt (metabolism)
• Signal Transduction (physiology)