The findings present the first evidence indicating that miR-23b can promote the proliferation, migration, and EMT of LECs by targeting SPRY2 and the inhibition of miR-23b may possess the therapeutic potential for cataract.
Taken together, our findings revealed that miR-23b-3p regulated apoptosis and autophagy via suppressing SIRT1 in LEC cell under oxidative stress, which could provide new ideas for clinical treatment of cataract.