ACTA ENDOCRINOLOGICA (BUC)

Objective. Insulinoma is one of the functional neuroendocrine tumors, which induce hypoglycemia caused by inadequate high secretion of insulin. In rats, two genes coding for insulin, insulin 1 (Ins1) and insulin 2 (Ins2) are found on chromosome 1. Some structural feature studies have shown that Ins1 was generated from a transcript of Ins2 and was inserted into the genome by an RNA-mediated duplication–transposition event. Methods. In this study, the author has investigated how the expression of insulin genes, Ins 1 and Ins2, are altered by Pdx-1 gene overexpression in the insulinoma cell line, Rin-5F. Results. Overexpression of the Pdx-1 gene increases Ins1 gene mRNA expression, not Ins2 gene mRNA expression, in the insulinoma cell line. Thus, levels of the rat insulin 1 and insulin 2 peptides may be changed under specific conditions. Conclusions. This is the first report that Ins1, but not Ins2, is significantly increased by Pdx-1 gene overexpression in the insulinoma cell line. This could indicate more research and analysis of insulinoma tumorigenesis and Pdx-1 gene expression.

Objective. One functional neuroendocrine tumor that causes hypoglycemia due to inappropriately high insulin production is an insulinoma. In rats, two genes coding for insulin, insulin 1 (Ins1) and insulin 2 (Ins2) are found on chromosome 1. Ins1 was produced from an Ins2 transcript, and it was inserted into the genome via an RNA-mediated duplication-transposition event, according to some structural feature analyses. Methods. In this study, the author has looked at how overexpression of the PTEN gene in the insulinoma cell line Rin- 5F affects the expression of the insulin genes, Ins 1 and Ins 2. Results. In the insulinoma cell line, overexpression of the PTEN gene boosts Ins2 gene mRNA expression but not Ins1 gene mRNA expression. It has been reported that PTEN upregulates insulin signaling by increasing insulin receptor substrate (IRS)-2 mRNA levels. Also, PTEN has been reported to be secreted in exosomes and thereafter, into extracellular space. Conclusions. The present study suggested that overexpression of PTEN might induce the increasing Ins 2 gene expression, one of the phosphorylated genes against the IRS-2 through the insulin/IGF-1 receptor. Our knowledge of the molecular pathways of PTEN relating the synthesis of insulin has been increased by the present study.