Wen Yuan, Dongxue Sun, Jing Wang, Yongli Yue, Xueling Li

State Key Laboratory of Reproductive Regulation and Breeding of Grassland Livestock, College of Life Science, Inner Mongolia University, Hohhot, 010021, People’s Republic of China

Correspondence: Yongli Yue, State Key Laboratory of Reproductive Regulation and Breeding of Grassland Livestock, College of Life Science, Inner Mongolia University, No. 24 Zhao Jun Road, Yu Quan Qu, Hohhot, Inner Mongolia, 010070, People’s Republic of China, Tel/Fax +86 471 3679873, Email yueyongli228@163.com Xueling Li, State Key Laboratory of Reproductive Regulation and Breeding of Grassland Livestock, College of Life Science, Inner Mongolia University, No. 24 Zhao Jun Road, Yu Quan Qu, Hohhot, Inner Mongolia, 010070, People’s Republic of China, Tel/Fax +86 471 3679807, Email lixueling@imu.edu.cn

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.

Keywords: MIN6 cells, Mi-Lnc70, apoptosis, G2/M arrest, insulin, glucagon