ArticleCells2022
TP53INP2 Contributes to TGF-β2-Induced Autophagy during the Epithelial-Mesenchymal Transition in Posterior Capsular Opacification Development.
Article in Cells, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 24 citations in OpenAlex.
- Micheliolide suppresses epithelial-mesenchymal transition of lens epithelial cells via downregulating matrix metalloproteinase 8 to ameliorate posterior capsular opacification.Journal of translational medicine · 2026Article
- HIF-3α Facilitates the Proliferation and Migration in Pancreatic Cancer by Inhibiting Autophagy Through Downregulating TP53INP2.Cell biochemistry and biophysics · 2025Article
- Promising Pharmacological Interventions for Posterior Capsule Opacification: A Review.Global challenges (Hoboken, NJ) · 2024Review
- Cytoplasmic TP53INP2 acts as an apoptosis partner in TRAIL treatment: the synergistic effect of TRAIL with venetoclax in TP53INP2-positive acute myeloid leukemia.Journal of experimental & clinical cancer research : CR · 2024Article
- TP53INP2 knockdown inhibits inflammatory response and apoptosis after spinal cord injury.Immunity, inflammation and disease · 2024Article
- Lens autophagy protein ATG16L1: a potential target for cataract treatment.Theranostics · 2024Article
- Review
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Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundPosterior capsule opacification (PCO) is the most common complication after cataract surgery, in which increased levels of transforming growth factor-beta 2 (TGF-β2) accelerate PCO formation; however, the pathological mechanisms are not fully understood. This study aims to explore the regulation mechanism of TGF-β2 in PCO formation via its autophagic functions.
methodsThe autophagic effect of TGF-β2 was detected by transmission electron microscopy (TEM), Western blotting, and immunofluorescence analysis. The association between autophagy and the epithelial-mesenchymal transition (EMT) was evaluated by qPCR and Western blotting. The transcriptome analysis was used to uncover the molecular mechanism of TGF-β2-induced PCO formation.
resultsTGF-β2 specifically promotes autophagy flux in human lens epithelial cells. The activation of autophagy by rapamycin can promote EMT marker synthesis and improve cell migration. However, the inhibition of autophagy by 3-MA attenuates EMT. To uncover the molecular mechanisms, we performed RNA sequencing and found that TGF-β2 elevated tumor protein p53-inducible nuclear protein2 (TP53INP2) expression, which was accompanied by a nuclear-to-cytoplasm translocation. Moreover, the knockdown of TP53INP2 blocked the TGF-β2-induced autophagy and EMT processes, revealing that TP53INP2 plays an important role in TGF-β2-induced autophagy during EMT.
conclusionsTaken together, the results of this study suggested that TP53INP2 was a novel regulator of PCO development by TGF-β2, and notably, TP53INP2, may be a potential target for the pharmacological treatment of PCO.
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