Diabetes, Metabolic Syndrome and Obesity (Jan 2022)
RNF6 Targeted by miR-26a-5p Protects Pancreatic β-Cell Function Against Type 2 Diabetes
Abstract
Fan Yang,1,* Shengxun Zhao,2,* Xuyan Zhang,3 Sheng Ding,3 Yancheng Xu1 1Department of Endocrinology, Wuhan University Zhongnan Hospital, Wuhan, 430000, Hubei, People’s Republic of China; 2Department of Geriatrics, The First Hospital of Wuhan, Wuhan, 430000, Hubei, People’s Republic of China; 3Department of Endocrinology, The Central Hospital of Wuhan, Wuhan, 430014, Hubei, People’s Republic of China*These authors contributed equally to this workCorrespondence: Yancheng XuDepartment of Endocrinology, Wuhan University Zhongnan Hospital, No. 169, Donghu Road, Wuchang District, Wuhan, 430000, Hubei, People’s Republic of ChinaTel +86 13907116967Email [email protected]: 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
