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

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

机构信息

Department of Otolaryngology, Eye & ENT Hospital, Fudan University, 83 Fenyang Road, Shanghai, China.

NHC Key Laboratory of Hearing Medicine (Fudan University), Shanghai, 200031, PR China.

出版信息

Int J Med Sci. 2021 Aug 2;18(15):3403-3411. doi: 10.7150/ijms.60617. eCollection 2021.

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 CoCl. The proliferation and cellular HIF-1α, p-PDK1 and p‑Akt expression levels of cholesteatoma keratinocytes were assessed . 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.

摘要

在此,我们旨在探讨缺氧是否通过 PI3K-Akt 信号级联触发胆脂瘤角质形成细胞的增殖。将细胞接种于不同浓度的 CoCl 中。评估胆脂瘤角质形成细胞的增殖以及细胞中 HIF-1α、p-PDK1 和 p-Akt 的表达水平。缺氧通过上调 p-PDK1 和 p-Akt 的表达来促进细胞增殖。PI3K-Akt 信号级联的特异性抑制剂 LY294002 显著抑制 p-Akt 的表达,并显著减少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生和进展。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eb2b/8436096/192d915e596a/ijmsv18p3403g001.jpg

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