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Background <p>Glaucoma is an irreversible blinding disease worldwide with complex pathogenesis. Previous studies have indicated that Specificity protein 1 (SP1) plays a critical role in diverse diseases, including glaucoma. This study is designed to explore the role and underlying mechanism of SP1 in the development of glaucoma.</p> Methods <p>SP1 and Snail Family Transcriptional Repressor 2 (SNAI2) levels were detected by real-time quantitative polymerase chain reaction (RT-qPCR). SP1, SNAI2, Fibronectin, α-SMA, E-cadherin, LC3BI, LC3BII, and p62 protein levels were assessed using western blot assay. Binding between SP1 and SNAI2 promoter was predicted by JASPAR and validated using Chromatin immunoprecipitation (ChIP) and dual-luciferase reporter assays. Cell viability, migration, and invasion were measured using Cell Counting Kit-8 (CCK-8), transwell, and wound healing assays.</p> Results <p>SP1 and SNAI2 were highly expressed in glaucoma patients and transforming growth factor beta-1 (TGF-β1)-treated human Tenon’s capsule fibroblast cells (HTFs). At the molecular level, SP1 was a transcription factor of SNAI2 and increased the transcriptional activity of SNAI2 by binding to its promoter region. SP1 knockdown could relieve TGF-β1-induced HTF viability, migration, invasion, extracellular matrix (ECM) deposition, and autophagy.</p> Conclusion <p>SP1-activated SNAI2 transcription promotes TGF-β1-triggered HTF viability, migration, invasion, ECM deposition, and autophagy, which provides a promising therapeutic target for glaucoma treatment.</p>

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Transcription factor SP1 drives TGF-β1-induced transformation of human tenon’s capsule fibroblasts by transcription activation-mediated SNAI2 upregulation

  • 期刊论文

  • 发表日期：

    2025年6月12日

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  • Yiying Chen,
  • Yirong Chen,
  • Chunmei Li,
  • Zongkai Bai,
  • Han Yang,
  • Qianqian Wang,
  • Yaqin Zhang

摘要

Background

Glaucoma is an irreversible blinding disease worldwide with complex pathogenesis. Previous studies have indicated that Specificity protein 1 (SP1) plays a critical role in diverse diseases, including glaucoma. This study is designed to explore the role and underlying mechanism of SP1 in the development of glaucoma.

Methods

SP1 and Snail Family Transcriptional Repressor 2 (SNAI2) levels were detected by real-time quantitative polymerase chain reaction (RT-qPCR). SP1, SNAI2, Fibronectin, α-SMA, E-cadherin, LC3BI, LC3BII, and p62 protein levels were assessed using western blot assay. Binding between SP1 and SNAI2 promoter was predicted by JASPAR and validated using Chromatin immunoprecipitation (ChIP) and dual-luciferase reporter assays. Cell viability, migration, and invasion were measured using Cell Counting Kit-8 (CCK-8), transwell, and wound healing assays.

Results

SP1 and SNAI2 were highly expressed in glaucoma patients and transforming growth factor beta-1 (TGF-β1)-treated human Tenon’s capsule fibroblast cells (HTFs). At the molecular level, SP1 was a transcription factor of SNAI2 and increased the transcriptional activity of SNAI2 by binding to its promoter region. SP1 knockdown could relieve TGF-β1-induced HTF viability, migration, invasion, extracellular matrix (ECM) deposition, and autophagy.

Conclusion

SP1-activated SNAI2 transcription promotes TGF-β1-triggered HTF viability, migration, invasion, ECM deposition, and autophagy, which provides a promising therapeutic target for glaucoma treatment.