SP1 promotes high glucose-induced lens epithelial cell viability, migration and epithelial-mesenchymal transition via regulating FGF7 and PI3K/AKT pathway.

IF 1.4 4区医学 Q3 OPHTHALMOLOGY

International Ophthalmology Pub Date : 2024-07-06 DOI:10.1007/s10792-024-03230-6

Ledan Wang, Xin Zhang, Huijun Li, Yuehong Mou, Gangfeng Cui

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Abstract

Background: Diabetic cataract (DC) is a common complication of diabetes and its etiology and progression are multi-factorial. In this study, the roles of specific protein 1 (SP1) and fibroblast growth factor 7 (FGF7) in DC development were explored.

Methods: DC cell model was established by treating SRA01/04 cells with high glucose (HG). MTT assay was conducted to evaluate cell viability. Transwell assay and wound-healing assay were performed to assess cell migration and invasion. Western blot assay and qRT-PCR assay were conducted to measure the expression of N-cadherin, E-cadherin, Collagen I, Fibronectin, SP1 and FGF7 expression. CHIP assay and dual-luciferase reporter assay were conducted to analyze the combination between FGF7 and SP1.

Results: FGF7 was upregulated in DC patients and HG-induced SRA01/04 cells. HG treatment promoted SRA01/04 cell viability, migration, invasion and epithelial-mesenchymal transition (EMT), while FGF7 knockdown abated the effects. Transcription factor SP1 activated the transcription level of FGF7 and SP1 overexpression aggravated HG-induced SRA01/04 cell injury. SP1 silencing repressed HG-induced SRA01/04 cell viability, migration, invasion and EMT, but these effects were ameliorated by upregulating FGF7. Additionally, SP1 knockdown inhibited the PI3K/AKT pathway by regulating the transcription level of FGF7.

Conclusion: Transcription factor SP1 activated the transcription level of FGF7 and the PI3K/AKT pathway to regulate HG-induced SRA01/04 cell viability, migration, invasion and EMT.

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SP1 通过调节 FGF7 和 PI3K/AKT 通路，促进高糖诱导的晶状体上皮细胞活力、迁移和上皮-间质转化。

背景：糖尿病性白内障（DC）是糖尿病的一种常见并发症，其病因和进展是多因素的。本研究探讨了特异性蛋白 1（SP1）和成纤维细胞生长因子 7（FGF7）在 DC 发育中的作用：方法：用高糖（HG）处理 SRA01/04 细胞，建立 DC 细胞模型。MTT 试验评估细胞活力。透孔试验和伤口愈合试验用于评估细胞迁移和侵袭。通过 Western 印迹和 qRT-PCR 检测 N-cadherin、E-cadherin、Collagen I、Fibronectin、SP1 和 FGF7 的表达。CHIP检测和双荧光素酶报告实验分析了FGF7和SP1的结合情况：结果：FGF7在DC患者和HG诱导的SRA01/04细胞中上调。HG处理促进了SRA01/04细胞的活力、迁移、侵袭和上皮-间质转化（EMT），而FGF7敲除则减轻了这些影响。转录因子 SP1 激活了 FGF7 的转录水平，SP1 的过表达加重了 HG 诱导的 SRA01/04 细胞损伤。沉默 SP1 可抑制 HG 诱导的 SRA01/04 细胞活力、迁移、侵袭和 EMT，但上调 FGF7 可改善这些影响。此外，SP1敲除可通过调节 FGF7 的转录水平抑制 PI3K/AKT 通路：结论：转录因子 SP1 可激活 FGF7 的转录水平和 PI3K/AKT 通路，从而调控 HG 诱导的 SRA01/04 细胞活力、迁移、侵袭和 EMT。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

International Ophthalmology OPHTHALMOLOGY-

CiteScore

3.20

自引率

0.00%

发文量

451

期刊介绍： International Ophthalmology provides the clinician with articles on all the relevant subspecialties of ophthalmology, with a broad international scope. The emphasis is on presentation of the latest clinical research in the field. In addition, the journal includes regular sections devoted to new developments in technologies, products, and techniques.