ArticleScientific reports2017
MicroRNA-30a Regulation of Epithelial-Mesenchymal Transition in Diabetic Cataracts Through Targeting SNAI1.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 55 citations in OpenAlex.
- Assessing the therapeutic effects of DPP4 Inhibitors on TGF-β2-induced Lens Opacity.Experimental eye research · 2026Article
- MicroRNA-204-5p Attenuates Oxidative Stress, Apoptosis and Inflammation by Targeting TXNIP in Diabetic Cataract.Biochemical genetics · 2025Article
- SP1 promotes high glucose-induced lens epithelial cell viability, migration and epithelial-mesenchymal transition via regulating FGF7 and PI3K/AKT pathway.International ophthalmology · 2024Article
- GDF-15 Attenuates the Epithelium-Mesenchymal Transition and Alleviates TGFβ2-Induced Lens Opacity.Translational vision science & technology · 2024Article
- Article
- MicroRNA-22-3p Regulates the Apoptosis of Lens Epithelial Cells Through Targeting KLF6 in Diabetic Cataracts.Translational vision science & technology · 2023Article
- The interaction between autophagy and the epithelial-mesenchymal transition mediated by NICD/ULK1 is involved in the formation of diabetic cataracts.Molecular medicine (Cambridge, Mass.) · 2022Article
- CircPAG1 interacts with miR-211-5p to promote the E2F3 expression and inhibit the high glucose-induced cell apoptosis and oxidative stress in diabetic cataract.Cell cycle (Georgetown, Tex.) · 2022Article
- Histone acetyltransferase inhibition reverses opacity in rat galactose-induced cataract.PloS one · 2022Article
- microRNA-199a-5p regulates epithelial-to-mesenchymal transition in diabetic cataract by targeting SP1 gene.Molecular medicine (Cambridge, Mass.) · 2020Article
- Let-7a-5p represses proliferation, migration, invasion and epithelial-mesenchymal transition by targeting Smad2 in TGF-b2-induced human lens epithelial cells.Journal of biosciences · 2020Article
- miR-30a reverses TGF-β2-induced migration and EMT in posterior capsular opacification by targeting Smad2.Molecular biology reports · 2019Article
- Cadmium exposure upregulates SNAIL through miR-30 repression in human lung epithelial cells.Toxicology and applied pharmacology · 2019Article
- microRNA-378a Regulates the Reactive Oxygen Species (ROS)/Phosphatidylinositol 3-Kinases (PI3K)/AKT Signaling Pathway in Human Lens Epithelial Cells and Cataract.Medical science monitor : international medical journal of experimental and clinical research · 2019Article
- Role ofOxidative medicine and cellular longevity · 2019Article
- Vimentin Diversity in Health and Disease.Cells · 2018Review
- Long noncoding RNA KCNQ1OT1 promotes proliferation and epithelial‑mesenchymal transition by regulation of SMAD4 expression in lens epithelial cells.Molecular medicine reports · 2018Article
- Identification of HBMC ophthalmology · 2018Article
- MiR-106a-5p inhibits the cell migration and invasion of renal cell carcinoma through targeting PAK5.Cell death & disease · 2017Article
- MiR-30a inhibits BECN1-mediated autophagy in diabetic cataract.Oncotarget · 2017Article
Corrections and comments
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Authors and funding
7 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Epithelial-mesenchymal transition (EMT) is a highly conserved and fundamental process in development, fibrosis, and metastasis. During the process, epithelial cells lose their morphology and transcriptional program, and transdifferentiate to mesenchymal cells. It has been reported that lens epithelial cells undergo EMT during cataract formation, and regulation of microRNAs on genes is associated with lens development. However, the molecular mechanisms of this regulation in diabetic cataract still need to be investigated. In the present study, the expression of E-cadherin was downregulated, while the expression of alpha-SMA and vimentin was upregulated in diabetic cataract tissues and the in vitro model, suggesting the involvement of EMT in diabetic cataract formation. Results of miRNA profiling demonstrated that miR-30a was markedly downregulated in diabetic cataract tissues. Overexpression of miR-30a-5p decreased SNAI1, a known modulator of EMT, and the expression of vimentin and alpha-SMA in our diabetic cataract model in vitro. It is concluded that EMT is involved in human diabetic cataract, and upregulation of miR-30a can repress EMT through its targeting of SNAI1 in lens epithelial cells, which make miR-30a a novel target of therapeutic intervention for human diabetic cataract.
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