Rapid Communication
Copyright ©2008 The WJG Press and Baishideng. All rights reserved.
World J Gastroenterol. May 14, 2008; 14(18): 2900-2904
Published online May 14, 2008. doi: 10.3748/wjg.14.2900
Primary study of leptin and human hepatocellular carcinoma in vitro
Jing Zhou, Wei Lei, Lei Shen, He-Sheng Luo, Zhi-Xiang Shen
Jing Zhou, Lei Shen, He-Sheng Luo, Zhi-Xiang Shen, Department of Gastroenterology, Renmin Hospital of Wuhan University, Wuhan 430060, Hubei Province, China
Wei Lei, Department of Urology, Wuhan Children Hospital, Wuhan 430016, Hubei Province, China
Author contributions: Zhou J, Shen L, Luo HS, and Shen ZX designed research; Zhou J and Lei W performed research; Zhou J and Lei W analyzed data; and Zhou J, Lei W and Shen ZX wrote the paper.
Correspondence to: Zhi-Xiang Shen, Department of Gastroenterology, Renmin Hospital of Wuhan University, No. 238 Jiefang Road, Wuchang District, Wuhan 430060, Hubei Province, China. nancy61317@163.com
Telephone: +86-27-62530538
Fax: +86-27-88042292
Received: January 9, 2008
Revised: March 21, 2008
Published online: May 14, 2008
Abstract

AIM: To investigate the expression level and effects of leptin in human hepatocellular carcinoma cells in vitro and to explore the correlation between them.

METHODS: Human hepatocellular carcinoma cell line HepG2 was cultured in vitro, and (the expression level) mRNA of leptin and leptin receptors in HepG2 were assessed using reverse transcription polymerase chain reaction (RT-PCR). Effects of different concentrations of leptin (50 ng/mL, 100 ng/mL, 200 ng/mL) on HepG2 were detected with colorimetric assay by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) after incubation periods of 24 h, 48 h, and 72 h. Flow cytometry was performed to assess cell cycle progression of different concentrations of leptin as stated above after each 24 h incubation period.

RESULTS: mRNA of leptin and leptin receptors (including short and long isoforms) were expressed in HepG2. The 72 h incubation of leptin at different concentrations (50 ng/mL, 100 ng/mL, 200 ng/mL) promoted proliferation of HepG2 in a concentration- and time-dependent manner. The experimental group shows significant statistical differences when compared to the controlled group which contained 0 ng/mL of leptin. As the concentration of leptin increases, significant fewer cells were detected in G0-G1 phase and more cells in S and G2-M phases.

CONCLUSION: Leptin and leptin receptor are simultaneously expressed in human hepatocellular carcinoma cell line HepG2. Addition of leptin (0 ng/mL-200 ng/mL) in 72 h periods indicated there is a concentration- and time-dependent correlation in the stimulation of HepG2 cell proliferation. The effect of proliferation by leptin is due to promotion of DNA synthesis and enhancement of mitotic activity. The relationship between leptin and human hepatocellular carcinoma cells might indicate that adipokine could be associated with the progression of human hepatocellular carcinoma.

Keywords: Leptin; Hepatocellular carcinoma; Proliferation