ArticleInternational journal of ophthalmology2021
miRNA-26b suppresses the TGF-β2-induced progression of HLE-B3 cells
Article in International journal of ophthalmology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 10 citations in OpenAlex.
- Crucial involvement of transforming growth factor beta (TGF-β)/Smad signaling regulation by miR-204-5p in cataract and posterior capsular opacification.Biochemistry and biophysics reports · 2026Review
- The regulation of placental pericyte function through transforming growth factor β-1 signalling.Scientific reports · 2025Article
- Expression of LncRNAs in anterior capsule of lens in patients with pathologic myopia complicated with cataract.International ophthalmology · 2024Article
- Promising Pharmacological Interventions for Posterior Capsule Opacification: A Review.Global challenges (Hoboken, NJ) · 2024Review
- Characterization of NInternational journal of ophthalmology · 2024Article
- Engineered exosomes enriched in netrin-1 modRNA promote axonal growth in spinal cord injury by attenuating inflammation and pyroptosis.Biomaterials research · 2023Article
- Role of reactive oxygen species in epithelial-mesenchymal transition and apoptosis of human lens epithelial cells.International journal of ophthalmology · 2023Article
- DHW-208, A Novel Phosphatidylinositol 3-Kinase (PI3K) Inhibitor, Has Anti-Hepatocellular Carcinoma Activity Through Promoting Apoptosis and Inhibiting Angiogenesis.Frontiers in oncology · 2022Article
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Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aimTo study the effect of miR-26b on lens epithelial cells induced by transforming growth factor beta (TGF-β) 2 and the underlying signaling pathways.
methodsHuman lens epithelial cell line B-3 (HLE-B3) was incubated with TGF-β2 (5 ng/mL) and then transfected with miR-26b mimics. The expression of miR-26b was determined using quantitative reverse transcriptase polymerase chain reaction (qRT-PCR), while 5'-bromodeoxyuridine (BrdU) and wound-healing assays were used to measure the growth and migration of HLE-B3 cells, respectively. The expression of epithelial-mesenchymal transition (EMT) markers and the activity of the phosphatidylinositol 3-kinase (PI3K)/Akt pathway were measured by Western blotting assay and immunofluorescence staining. Electron microscopy was also used to observe cellular morphology.
resultsThe expression levels of miR-26b were significantly reduced in human posterior capsular opacification-attached lens tissue and TGF-β2-stimulated HLE-B3 cells. In the presence of TGF-β2, the growth, migration, and EMT of HLE-B3 cells were distinctly enhanced; these effects were attenuated by the administration of miR-26b mimics. Furthermore, the overexpression of miR-26b significantly reduced upregulation of the PI3K/Akt pathway when stimulated by TGF-β2 in HLE-B3 cells. Moreover, the addition of an activator (740 Y-P) led to the upregulation of the PI3K/Akt pathway and abolished the protective effect of miR-26b on the HLE-B3 cells that was mediated by TGF-β2.
conclusionThe miR-26b suppresses TGF-β2-induced growth, migration, and EMT in HLE-B3 cells by regulating the PI3K/Akt signaling pathway.
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