Abstract
The tumor suppressor protein ELL-associated factor 2 (Eaf2) serves an important role in lens development and maturation; however, its role in oxidative stress‑induced cataract formation remains unclear. In the present study, an in vitro apoptosis model was constructed by treating HLE‑B3 cells with 50 µM hydrogen peroxide (H2O2), and was confirmed by flow cytometry. Subsequently, overexpression of Eaf2 was induced in H2O2‑induced HLE‑B3 cells by ligating Eaf2 cDNA to a pcDNA3.0 plasmid and the role of Wnt3a in the function of Eaf2 was also assessed by inhibiting the expression of the gene in Eaf2‑overexpression cells. The expression levels of glycogen synthase kinase 3β, β‑catenin, Eaf2, caspase 3, Wnt3a, B‑cell lymphoma 2 (Bcl‑2) and Bcl‑2‑associated X protein were examined using reverse transcription‑quantitative polymerase chain reaction and western blot analysis. Immunocytochemistry was used to locate Eaf2 and Wnt3 protein expression in the H2O2‑induced HLE‑B3 cells. The results indicated that Eaf2 was able to effectively suppress H2O2‑induced apoptosis of HLE cells via inhibition of caspase 3 production and activation of Wnt3a signaling. In addition, knockdown of Wnt3a in Eaf2‑overexpression cells evidently counteracted the effect of Eaf2 in antagonizing H2O2‑induced apoptosis. Taken together, these findings suggested that Eaf2 may suppress oxidative stress‑induced apoptosis of HLE‑B3 cells exerted through the activation of Wnt3a signaling.