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

被引：13

作者：

Chowdhury, Md. Kamrul H. ^{[1
]}

Montgomery, Magda K. ^{[1
]}

Morris, Margaret J. ^{[1
]}

Cognard, Emmanuelle ^{[2
]}

Shepherd, Peter R. ^{[2
]}

Smith, Greg C. ^{[1
]}

机构：

[1] UNSW Australia, Dept Pharmacol, Sydney, NSW, Australia

[2] Univ Auckland, Dept Mol Med & Pathol, Auckland 1, New Zealand

来源：

ARCHIVES OF PHYSIOLOGY AND BIOCHEMISTRY | 2015年 / 121卷 / 03期

关键词：

beta-Catenin; cancer; glucagon; T2D; PREEXISTING DIABETES-MELLITUS; CANCER-RISK; COLORECTAL-CANCER; HEPATOCELLULAR CARCINOMAS; INSULIN-RESISTANCE; MOLECULAR LINKS; PROSTATE-CANCER; KIDNEY CANCER; GLUCOSE; METAANALYSIS;

D O I：

10.3109/13813455.2015.1048693

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

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/beta-catenin pathway. In this study, we aimed to identify the effect of glucagon on beta-catenin in the isolated rat liver. We found glucagon, which is substantially raised in patients with T2D, rapidly phosphorylates beta-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.

引用

页码：88 / 96

页数：9

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