Association Between Proteasome 26S Subunit, Non-ATPase 3 Methylation and Insulin β Cell Apoptosis in Type 2 Diabetic Mellitus.

BACKGROUND

The methylation of and its influence on protein stability and degradation could play a crucial role in the pathogenesis of type 2 diabetes mellitus (T2DM), although the underlying molecular mechanisms are not yet fully understood. This study investigates the molecular and bioinformatic features of methylation in T2DM.

METHODS

Bioinformatics analyses were conducted on the T2DM database chip. A model of T2DM was established in rat RIN-m5F cells induced by high glucose (HG) concentration. The function of the gene in T2DM was examined through its overexpression. Western blotting was used to detect the expression of and USP14 proteins. Flow cytometry was used to detect cell apoptosis and proliferation.

RESULTS

Methylation of was upregulated in the T2DM tissue microarray data and associated with USP14. overexpression reduced apoptosis and enhanced proliferation in HG-treated RIN-m5F cells. In HG-treated RIN-m5F cells, was linked to USP14 inactivation.

CONCLUSION

methylation might potentially influences cell apoptosis and proliferation in T2DM development which might be associated with activating USP14. This study offers an in-depth examination of methylation's molecular and bioinformatic traits in T2DM, advancing our comprehension of the molecular mechanisms leading to T2DM.