目的:肝癌的转移与复发是肝癌治疗的一大难题,盐霉素是近年来新发现的具有抗肿瘤作用的抗生素,本文研究了盐霉素在体外及体内对人肝细胞癌转移与侵袭能力的作用及机制。方法:在体外对肝癌细胞株HepG2,SMMC-7721,BEL-7402给予盐霉素处理,体内建立裸鼠肝脏原位肿瘤模型,并给予腹腔注射盐霉素治疗。观察肿瘤细胞的转移侵袭能力以及肝内肿瘤转移灶的情况,进一步测定E.cadherin,Vimentin的表达,来研究盐霉素对肝癌转移及侵袭能力的影响及机制。结果:经盐霉素处理后,肝癌细胞株HepG2,SMMC.7721,BEL.7402的转移及侵袭能力明显下降,肝内转移灶的数目也减少。分子机制检测发现盐霉素处理后E.cadherin表达增高,Vimentin表达下降。结论:盐霉素在体内与体外都抑制了肝癌的转移与侵袭,其机制可能抑制了肿瘤细胞的上皮间质化(EMT)过程。这为控制肝癌的转移和复发提供了新的治疗思路。
Objective: Metastasis and recurrence are the major problems of the treatment of liver cancer. Salinomycin is a antitumor antibiotic discovered in recent years, this study aimed to research the effects and mechanism of salinomycin on the metastasis and invasion of human hepatocellular carcinoma in vitro and in vivo. Methods: Salinomycin treated hepatocellular carcinoma cell lines HepG2, SMMC-7721, BEL-7402 in vitro and nude mice hepatoma orthotopic tumor model in vivo. The ability of metastasis and invasion of hepatocellular carcinoma cells and the number of hepatoma tumor metastasis were observed. Furthermore, the expression of E-cadhedn and Vimentin were determined to study the mechanism of salinomycin effects on the metastasis and invasion of hepatoma carcinoma. Results: After salinomycin treatment, the metastasis and invasion of hepatocellular carcinoma cell lines HepG2, SMMC-7721, BEL-7402 were decreased, also the number of hepatoma tumor metastasis reduced. Salinomycin treatment increased the expression of E-cadherin, decreased the expression of Vimentin. Conclusion: Salinomycin in vitro and in vivo inhibits metastasis and invasion of hepatocellular carcinoma, the mechanism may be the inhibition the process of epithelial- mesenchymal transition (EMT). This provides us a new therapeutic idea for the metastasis and recurrence of HCC.