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抑制高迁移率族蛋白 B1/晚期糖基化终末产物受体(HMGB1/RAGE)轴抑制脂多糖(LPS)诱导的宫颈上皮细胞的恶性转化。

Inhibition of HMGB1/RAGE axis suppressed the lipopolysaccharide (LPS)-induced vicious transformation of cervical epithelial cells.

机构信息

Department of Gynecology, First People's Hospital of Yuhang District, Hangzhou, China.

Laboratory Department, First People's Hospital of Yuhang District, Hangzhou, China.

出版信息

Bioengineered. 2021 Dec;12(1):4995-5003. doi: 10.1080/21655979.2021.1957750.

Abstract

The chronic inflammation operates as one of the critical causes of cervical cancer. Activation of HMGB1/RAGE axis could induce the inflammation and lead to multiple types of cancer. However, whether the HMGB1/RAGE axis could affect the development of cervical cancer by regulating the inflammation is unclear. Here, we stimulated normal cervical epithelial cells with lipopolysaccharide (LPS). Next, the expression of RAGE in these cells was suppressed by the RAGE inhibitor. CCK-8 and wound healing assays were performed to detect the proliferation and invasion. To determine how inflammatory factors (IL-1β, IL-6 and TNF-α) expressed in supernatant of these cells, ELISA was conducted. Western blotting was used for the detection of the expression of pyroptosis-related proteins (NLRP3 and caspase4). It was found that stimulation of LPS enhanced the proliferation and invasion of normal cervical epithelial cells. The expression of inflammatory factors (IL-1β, IL-6 and TNF-α) in these cells was promoted as well. Application of RAGE inhibitor abolished the efficacy of LPS on these cells. Furthermore, LPS promoted the expression of NLRP3 and caspase4 in these cells while RAGE inhibitor exerted suppressive effects on the expression of these proteins. In summary, LPS-induced inflammation of normal cervical epithelial cells resulted in the malignant transformation of these cells by activating HMGB1/RAGE axis.

摘要

慢性炎症是宫颈癌的一个重要原因。HMGB1/RAGE 轴的激活可诱导炎症,导致多种癌症。然而,HMGB1/RAGE 轴是否可以通过调节炎症来影响宫颈癌的发展尚不清楚。在这里,我们用脂多糖(LPS)刺激正常宫颈上皮细胞。然后,用 RAGE 抑制剂抑制这些细胞中 RAGE 的表达。通过 CCK-8 和划痕愈合实验检测细胞的增殖和侵袭。为了确定这些细胞上清液中表达的炎性因子(IL-1β、IL-6 和 TNF-α),我们进行了 ELISA 实验。通过 Western blot 检测细胞中细胞焦亡相关蛋白(NLRP3 和 caspase4)的表达。结果发现,LPS 的刺激增强了正常宫颈上皮细胞的增殖和侵袭。这些细胞中炎性因子(IL-1β、IL-6 和 TNF-α)的表达也得到了促进。RAGE 抑制剂的应用消除了 LPS 对这些细胞的作用。此外,LPS 促进了这些细胞中 NLRP3 和 caspase4 的表达,而 RAGE 抑制剂对这些蛋白的表达有抑制作用。总之,LPS 诱导正常宫颈上皮细胞的炎症通过激活 HMGB1/RAGE 轴导致这些细胞的恶性转化。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/163e/8806497/616277ca8a26/KBIE_A_1957750_F0001_OC.jpg

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