Inhibition of circular RNA 006029 alleviates pancreatic β-cell injury through the AKT/mTOR signaling pathway

Type 1 diabetes mellitus (T1DM) is characterized by the damage of pancreatic β-cells induced by autoimmune responses. Circular RNAs (circRNAs) serve important regulatory functions in the pathogenesis of T1DM, but the underlying mechanisms require more substantiation. This study focused on a novel circRNA circ006029 to investigate its regulations on β-cell damage. The potential involvement of circ006029 in β-cell proliferation, apoptosis, autophagy, and inflammatory responses was investigated via experiments such as CCK-8, qRT-PCR, and immunoblot. The utilization of a cytokine mixture, and specific molecular blockers Rapamycin and Capivasertib were applied to investigate the pathway by which circ006029 regulates in β-cell damage. Transcriptome sequencing and bioinformatics analysis were conducted to explore differentially expressed mRNAs related to circ006029 regulation. The expression of circ006029 was observed to increase in damaged MIN6 cells. The inhibition of circ006029 serves a protective role in MIN6 β-cells by promoting β-cell proliferation and attenuating apoptosis. circ006029-knockdown could augment β-cell autophagy and attenuate apoptosis through the AKT/mTOR signaling pathway. Moreover, circ006029 might be involved in the inflammatory response of MIN6 cells. These findings suggest that circ006029 may serve a detrimental role in β-cell damage, which provides new ideas for exploring the mechanism of β-cell damage in early insulitis in T1DM.