AI Article Synopsis
- Abnormal growth and transformation of lens epithelial cells (LECs) lead to vision loss from posterior capsular opacification (PCO) following cataract surgery.
- Overexpression of insulin-like growth factor-1 (IGF-1) promotes LEC proliferation, migration, and epithelial-mesenchymal transition (EMT), while reducing IGF-1 inhibits these processes.
- The microRNA miR-3666 was identified as a potential regulator of IGF-1, showing that it can suppress LEC malignant behaviors and offers new therapeutic strategies for PCO prevention.
Article Abstract
The abnormal proliferation, migration, and epithelial-mesenchymal transformation (EMT) of lens epithelial cells (LECs) are the main reasons for vision loss caused by posterior capsular opacification (PCO) after cataract surgery. Insulin-like growth factor-1 (IGF-1) was found to be associated with the pathogenesis of cataracts, but its biological role in PCO is poorly understood. In the present study, IGF-1 overexpression facilitated the proliferation, migration, and EMT, whereas knockdown of IGF-1 markedly suppressed the proliferation, migration, and TGF-2-induced EMT of LECs. Additionally, to evaluate valuable microRNAs (miRNAs) which target IGF-1 to modulate LEC-EMT, we predicted miR-3666 might regulate IGF-1 by binding its 3'UTR according to the bioinformatics database. Furthermore, we verified that miR-3666 directly targeted IGF-1 by luciferase reporter assay. By using miR-3666 mimics, cell proliferation, migration, and invasion were suppressed, while being enhanced by the reduction of miR-3666. Knockout of IGF1 reverses the effect of the miR-3666 inhibitor on the malignant behavior of LECs. These results indicate the role of miR-3666/IGF-1 in LEC-EMT that offers new strategies for the therapy and prevention of PCO.
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|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC9303496 | PMC |
| http://dx.doi.org/10.1155/2022/5383146 | DOI Listing |
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