Recently, microRNAs (miRNAs) receive more attention due to their role in the pathogenesis of malignancies. Retinoblastoma (RB) is the most serious and harmful malignant tumor in infants and young children with eye diseases, which often endangers the lives of children. This study was designed to determine how miR-598 is involved in RB progression. In this study, quantitative reverse transcription-polymerase chain reaction, Western blot, dual-luciferase reporter, Cell Counting Kit-8, and Transwell assays were adopted to detect miR-598 expression and function in RB. The decreased expression of miR-598 was identified in RB. Overexpression of miR-598 suppressed the viability and metastasis of RB cells. Further, E2F transcription factor 1 (E2F1) is verified as a direct target of miR-598. Furthermore, E2F1 recovered miR-598-mediated-inhibition of cell viability and metastasis in RB. In addition, miR-598 was found to promote cell apoptosis and inactivate the protein kinase B (AKT) pathway in RB. miR-598 suppressed RB cell viability and metastasis through inhibiting E2F1 and inactivating AKT pathway, which may provide a new perspective for RB treatment.
Diabetic retinopathy is the most important ocular complication associated with diabetes. Corneal defects due to diabetes mellitus ( DM ) may cause severe vision impairments. This study aimed to identify the effect of transforming growth factor‐β ( TGF ‐β) on biological events, such as apoptosis and inflammation, in the diabetic cornea. High‐glucose treatment induced reactive oxygen species ( ROS ) production and several biological events, including apoptosis and inflammatory cytokine secretion, in human corneal epithelial cells. However, administration of TGF ‐β significantly decreased ROS production, Annexin V‐positive cells, and levels of inflammatory cytokines. Sprague Dawley rats were injected with streptozotocin (STZ) as a model of DM . Inflammatory cytokine secretion, apoptosis, and inflammation were all increased by STZ treatment. However, apoptosis and inflammation were markedly reduced following TGF ‐β treatment. In conclusion, TGF ‐β can ameliorate the enhancement of apoptosis and inflammation in diabetic cornea in in vivo and in vitro .
The aim of the present study was to explore the etiology of subconjunctival fibrosis (SCF) induced by ethylparaben, the most prevalent preservative in Chinese eye drops. Ethylparaben was administered to the left eyes of male Sprague-Dawley rats in the experimental group twice daily for 1 month, whereas the control group received PBS. Experimental group rats displayed a mild promotion in density of fibroblasts and a tighter deposition of collagen in the bulbar subepithelial connective tissue compared with the control group. Furthermore, the present findings revealed that extracellular matrix expression was promoted in murine bulbar conjunctival tissues in the experimental group. In primary conjunctival fibroblasts, expression of ECM triggered by ethylparaben was suppressed by XAV-939. Furthermore, stimulation of the Wnt/β-catenin axis triggered by ethylparaben was impaired by XAV-939. In conclusion, SCF triggered by ethylparaben results from extra ECM generation of conjunctival fibroblasts via the Wnt/β-catenin axis.
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