Open AccessLeptin receptor mediates the proliferation and glucose metabolism of pancreatic cancer cells via AKT pathway activation
Author(s) -
Yingjie Xu,
Meiyu Tan,
Xiaoyu Tian,
Jun Zhang,
Jie Zhang,
Jiajie Chen,
Weihong Xu,
Huiming Sheng
Publication year - 2019
Publication title -
molecular medicine reports
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.727
H-Index - 56
eISSN - 1791-3004
pISSN - 1791-2997
DOI - 10.3892/mmr.2019.10855
Subject(s) - leptin , endocrinology , medicine , protein kinase b , leptin receptor , biology , cancer cell , adipokine , cell growth , cancer research , chemistry , signal transduction , microbiology and biotechnology , cancer , biochemistry , obesity
Pancreatic cancer (PC) is the fourth leading cause of cancer‑related mortality worldwide. Leptin is an adipokine that is significantly increased in obese patients and that functions in various biological processes of cancer, such as tumor growth and metastasis. However, its role in PC cell proliferation and glucose metabolism and the underlying mechanisms remain unclear. In the present study, in vitro leptin treatment significantly promoted cell proliferation and increased glucose uptake and lactate production of human PC and healthy pancreas cells in a dose‑dependent manner, accompanied by increased expression of the glycolytic enzymes hexokinase II and glucose transporter 1. Furthermore, leptin receptor‑specific short hairpin RNAs were used to silence leptin receptor expression in PC cells, which had the opposite effect to leptin stimulation and decreased AKT phosphorylation. In addition, the effects of leptin stimulation were significantly counteracted by the AKT inhibitor LY294002, whereas the effects of leptin silencing were counteracted by AKT activator insulin‑like growth factor 1. The results of the present study suggested that leptin may contribute to cell proliferation and glucose metabolism of human PC cells, which may be through activation of the AKT pathway.