METTL16 Inhibits Lens Epithelial Cells Function in Diabetic Cataract via m6A-Modified DKK1-Mediated Wnt/β-Catenin Signaling.

ABSTRACT:

Purpose

To explore the role of methyltransferase-like protein 16 (METTL16), an N6-methyladenosine (m6A) methyltransferase, in the development and progression of diabetic cataracts (DCs), as its underlying molecular mechanisms remain unknown.

Methods

We evaluated m6A methylation levels in total RNA isolated from DC anterior capsule tissue and high glucose (HG)-induced human lens epithelial cells (HLECs) using m6A quantification and dot blot analysis. The expression levels of METTL16 in the anterior capsule tissue were detected using western blot analysis. Methylated RNA immunoprecipitation (MeRIP), RNA stability assays, and other relevant experiments were performed to investigate the regulatory mechanisms of METTL16 on methylation levels in HLECs. Additionally, cellular funct

SUBMITTER: Zhang B 

PROVIDER: S-EPMC12782201 | biostudies-literature | 2026 Jan

REPOSITORIES: biostudies-literature