Mechanism of Chemotactic Factor CCL5/RANTES in Diabetic Patients with Hepatic Carcinoma

Objective To observe the mRNA expression level of chemotactic factor CCL5 in human hepatoma cell line HepG2 and murine cell line H22 cultured with different concentrations of glucose,and to compare the tumorigenicity of H22 cell line in diabetic mice and normal mice, as well as to explore the mechanisms of CCL5 in diabetic patients with hepatic carcinoma. Methods Human hepatoma HepG2 cells and murine hepatoma H22 cells were cultured in vitro with different concentrations of glucose, 5.5 and 25 mmol/L. The migration of cells was determined by scratch assay. The total RNA of HepG2 and H22 cells cultured with different concentrations of glucose were extracted respectively.The mRNA expression level of chemotactic factor CCL5 was detected by RT-PCR method.After the mouse model of diabetes mellitus was established, we compared the tumorigenicity between diabetic mice and normal mice,and detect the expression levels of CCL5 in tumor tissues by immunohistochemistry assay. Results The migration of HepG2 cells was enhanced with the increase of glucose concentration in the medium. The mRNA expression levels of CCL5 in HepG2 and H22 cells cultured with high concentration of glucose were relatively higher than that with low concentration of glucose.The tumorigenicity speed of murine cells H22 in diabetic mice was faster than that with normal mice. The expression level of CCL5 in tumor tissues of diabetic mice was more than that of mice with normal glucose (P<0.05). Conclusion HepG2 and H22 cells cultured with high concentration of glucose could increase the expression level of CCL5. High blood glucose could cause an increased risk of hepatic carcinoma and accelerate the tumor growth. The chemotactic factor CCL5 might play a role in the growth and migration of hepatic carcinoma caused by diabetes mellitus.