Glucagon phosphorylates serine 552 of β-catenin leading to increased expression of cyclin D1 and c-Myc in the isolated rat liver. (July 2015)

• Record Type: Journal Article
• Authors: Chowdhury, Md. Kamrul H.; Montgomery, Magda K.; Morris, Margaret J.; Cognard, Emmanuelle; Shepherd, Peter R.; Smith, Greg C.
• Is Part Of: Archives of physiology and biochemistry. Volume 121:Number 3(2015)
• Page Start: 88
• Page End: 96
• Publication Date: 2015-07
• Subjects: Physiology -- Periodicals; Biochemistry -- Periodicals; Biophysics -- Periodicals; Biochemistry; Physiology; 571
• DOI: 10.3109/13813455.2015.1048693
• Languages: English
• ISSNs: 1381-3455

Abstract

<abstract> <title>Abstract</title> <p>In the last 20 years the prevalence of metabolic disorders, in particular type 2 diabetes (T2D), has more than doubled. Recently, a strong link between T2D and cancer, in particularly liver cancer has been reported. However, the mechanism connecting the development of type 2 diabetes and cancer remains unknown. One of the biggest drivers of liver cancer is alterations in the Wnt/β-catenin pathway. In this study, we aimed to identify the effect of glucagon on β-catenin in the isolated rat liver. We found glucagon, which is substantially raised in patients with T2D, rapidly phosphorylates β-catenin on serine 552 that is associated with increased expression of genes cyclin D1 (CCND1) and c-Myc (MYC), which are known to be involved in liver cancer. This finding may explain the increased risk of liver cancer in people with T2D.</p> </abstract>