Mi-Lnc70 Regulates the Progression of Murine Pancreatic β-Cell Line and Affects the Synthesis of Insulin and Glucagon.

BACKGROUND

Insulinoma, the most common type of pancreatic endocrine tumor, frequently induces hypoglycemia due to persistent hyperinsulinemia. Although Mi-Lnc70 expression progressively increases during pancreatic maturation in mice, the biological role of Mi-Lnc70 in pancreatic β cells remains elusive.

AIM

This study was designed to investigate the role of LncRNA-Mi-Lnc70 in the mouse pancreatic β-cell line MIN6.

METHODS

We performed quantitative real-time PCR, cell counting kit-8 (CCK-8) assay, flow cytometry, transwell assay, wound healing assay, immunofluorescence staining, and Western blotting.

RESULTS

The expression of Mi-Lnc70 was markedly elevated in mouse pancreatic β-cells (MIN6) compared to normal cells. Knockdown of Mi-Lnc70 markedly suppressed the proliferation, migration, and invasion capabilities of MIN6 cells but induced cell apoptosis and triggered G2/M phase cell cycle arrest. Moreover, Mi-Lnc70 knockdown influenced the expression profiles of pancreas-related lncRNAs and miRNAs and decreased the expression of islet-related genes and reduced the protein synthesis of INSULIN, GLUCAGON, and PDX1.

CONCLUSION

Mi-Lnc70 plays an important role in the proliferation, migration, and endocrine-related gene expression in pancreatic MIN6 cells, particularly in the synthesis of PDX1, INSULIN, and GLUCAGON.