Leptin regulates proliferation and apoptosis of colorectal carcinoma through PI3K/Akt/mTOR signalling pathway

Journal of biosciences

Zhi Duan³  Jian Chen²  Meiyan Wei³  Qimei Xu³  Meizuo Zhong1¹  Lianghua Wang³  Di Wang¹  Hui Chen³ 

[1] Departments of Cancer, Xiangya Hospital, Central South University, Changsha 410008, PR, China$$;Department of General Surgery, The First Hospital of Changsha, Changsha 410005, PR, China$$;Department of Pathology, The First Hospital of Changsha, Changsha 410005, PR, China$$

关键词: Colorectal carcinoma;    HCT-116;    leptin;    mammalian target of rapamycin (mTOR);    phosphatidylinositol 3-kinase PI3K;   

DOI  :  

来源: Indian Academy of Sciences

【 摘 要 】

Epidemiological studies have indicated that obesity is associated with colorectal cancer. The obesity hormone leptin is considered as a key mediator for cancer development and progression. The present study aims to investigate regulatory effects of leptin on colorectal carcinoma. The expression of leptin and its receptor Ob-R was examined by immunohistochemistry in 108 Chinese patients with colorectal carcinoma. The results showed that leptin/Ob-R expression was significantly associated with T stage, TNM stage, lymph node metastasis, distant metastasis, differentiation and expression of p-mTOR, p-70S6 kinase, and p-Akt. Furthermore, the effects of leptin on proliferation and apoptosis of HCT-116 colon carcinoma cells were determined. The results showed that leptin could stimulate the proliferation and inhibit the apoptosis of HCT-116 colon cells through the PI3K/Akt/mTOR pathway. Ly294002 (a PI3K inhibitor) and rapamycin (an mTOR inhibitor) could prevent the regulatory effects of leptin on the proliferation and apoptosis of HCT-116 cells via abrogating leptin-mediated PI3K/Akt/mTOR pathway. All these results indicated that leptin could regulate proliferation and apoptosis of colorectal carcinoma through the PI3K/Akt/mTOR signalling pathway.

【 授权许可】

Unknown