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miR-26a-5p 靶向 RNF6 保护胰腺 β 细胞功能对抗 2 型糖尿病
Authors Yang F, Zhao S, Zhang X, Ding S, Xu Y
Received 23 August 2021
Accepted for publication 17 December 2021
Published 11 January 2022 Volume 2022:15 Pages 93—102
DOI https://doi.org/10.2147/DMSO.S335088
Checked for plagiarism Yes
Review by Single anonymous peer review
Peer reviewer comments 2
Editor who approved publication: Prof. Dr. Antonio Brunetti
Background: Type 2 diabetes (T2D) is characterized by progressive β-cell dysfunction. Regulatory microRNAs (miRNAs) may be associated with this.
Methods: Serum miR-26a-5p and RNF6 levels were detected in T2D patients and healthy volunteers via qRT-PCR. Subsequently, the role of specific dysregulated miR-26a-5p or RNF6 in regulating insulin content, cell proliferation, and apoptosis was studied in INS-1 cells. The targeting correlation between miR-26a-5p and RNF6 was detected using a luciferase assay.
Results: RNF6 expression was significantly decreased in T2D individuals and INS-1 cells treated with high glucose, while miR-26a-5p expression was increased. In INS-1 cells, RNF6 overexpression or miR-26a-5p downregulation significantly increased insulin content and secretion, induced proliferation, and inhibited apoptosis. RNF6 has been identified as an miR-26a-5p target, which negatively regulates RNF6 to worsen INS-1 cell function.
Conclusion: RNF6 promoted insulin secretion and induced cell proliferation in INS-1 cells. This may be related to miR-26a-5p targeting and negatively regulating T2D pathogenesis.
Keywords: RNF6, miR-26a-5p, pancreatic, β-cell, type 2 diabetes, INS-1