RNF6 Targeted by miR-26a-5p Protects Pancreatic β-Cell Function Against Type 2 Diabetes

Abstract

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

Data Sharing Statement

The datasets used and/or analyzed during the current study are available from the corresponding author on reasonable request.

Ethics Approval and Informed Consent

The present study was approved by the Ethics Committee of the Wuhan University Zhongnan Hospital (Wuhan, China). The processing of clinical tissue samples is in strict compliance with the ethical standards of the Declaration of Helsinki. All patients signed written informed consent.

Consent for Publication

Consent for publication was obtained from the participants.

Consent to Participate

All patients signed written informed consent.

Disclosure

The authors declare that they have no conflict of interests.

Additional information

Funding

The authors disclosed receipt of the following financial support for the research, authorship, and/or publication of this article: This work was supported by National Natural Science Foundation of China (81970718).