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FOXM1和AURKB在调节银屑病角质形成细胞功能中的作用。

Role of FOXM1 and AURKB in regulating keratinocyte function in psoriasis.

作者信息

Zhao Zhaofeng, Cheng Jie, Hou Qiang, Zhu Jian, Chen Tu, Lu Sheng, Wu Guiju, Lv Hongli, Wu Xiujuan

机构信息

Central Laboratory, Shanghai Xuhui Central Hospital, Zhongshan-Xuhui Hospital, Fudan University, Shanghai, 200031, P.R. China.

Department of Urology, Shanghai Xuhui Central Hospital, Zhongshan-Xuhui Hospital, Fudan University, Shanghai, 200031, P.R. China.

出版信息

Open Med (Wars). 2024 Sep 30;19(1):20241049. doi: 10.1515/med-2024-1049. eCollection 2024.

Abstract

OBJECTIVE

This study investigated the effect of forkhead box M1 (FOXM1) and Aurora kinase B (AURKB) on the epidermal function of keratinocytes.

METHODS

Bioinformatics analysis was used to analyze the co-expression network of FOXM1 and its correlation with AURKB. The expression of FOXM1 and AURKB in tissues and cells was detected by immunofluorescence and real-time quantitative polymerase chain reaction, respectively. HaCaT cells were transfected with si-FOXM1 to knock down FOXM1. Cell proliferation was detected by cell counting kit-8 assay. Cell migration was detected by scratch assay. Cell invasion was detected by the Transwell invasion assay. Cell apoptosis and cell cycle were detected by flow cytometry.

RESULTS

FOXM1 and AURKB were positively correlated and highly expressed in psoriatic lesions. After transfection of si-FOXM1, the expression levels of FOXM1 and AURKB genes significantly decreased. The proliferation of HaCaT cells decreased, the apoptosis rate increased significantly, and the proportion of cells in the G1 phase increased significantly, while the proportion of cells in the S phase decreased significantly. The scratch closure of HaCaT cells was reduced, and the number of cell invasions decreased significantly.

CONCLUSION

FOXM1 and AURKB may affect the progression of psoriasis by regulating the proliferation, cell cycle, migration, and invasion of keratinocytes.

摘要

目的

本研究调查了叉头框M1(FOXM1)和极光激酶B(AURKB)对角质形成细胞表皮功能的影响。

方法

采用生物信息学分析来分析FOXM1的共表达网络及其与AURKB的相关性。分别通过免疫荧光和实时定量聚合酶链反应检测组织和细胞中FOXM1和AURKB的表达。用si-FOXM1转染HaCaT细胞以敲低FOXM1。通过细胞计数试剂盒-8检测法检测细胞增殖。通过划痕试验检测细胞迁移。通过Transwell侵袭试验检测细胞侵袭。通过流式细胞术检测细胞凋亡和细胞周期。

结果

FOXM1和AURKB呈正相关且在银屑病皮损中高表达。转染si-FOXM1后,FOXM1和AURKB基因的表达水平显著降低。HaCaT细胞的增殖减少,凋亡率显著增加,G1期细胞比例显著增加,而S期细胞比例显著降低。HaCaT细胞的划痕愈合减少,细胞侵袭数量显著减少。

结论

FOXM1和AURKB可能通过调节角质形成细胞的增殖、细胞周期、迁移和侵袭来影响银屑病的进展。

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