论文部分内容阅读
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: Liver cancer metastasis and recurrence is a major problem in the treatment of liver cancer. Salinomycin is a newly discovered antibiotic with anti-tumor effect in recent years. In this paper, the ability of salinomycin to invade and invade human hepatocellular carcinoma The role and mechanism. Methods: Hepatocellular carcinoma cell lines HepG2, SMMC-7721 and BEL-7402 were treated with salinomycin in vitro, and the model of orthotopic liver tumor in nude mice was established in vivo. Salinomycin was administered intraperitoneally. To observe the metastasis and invasion of tumor cells and metastasis of intrahepatic metastasis, and to further determine the expression of E-cadherin and Vimentin in order to study the effect and mechanism of salinomycin on the metastasis and invasion of liver cancer. Results: After salinomycin treatment, the metastatic and invasive ability of HepG2, SMMC-7721 and BEL-7402 cells were significantly decreased, and the number of liver metastases was also decreased. Molecular mechanism detection found salinomycin treatment E-cadherin expression increased, Vimentin expression decreased. Conclusion: Salinomycin can inhibit the metastasis and invasion of hepatocellular carcinoma both in vitro and in vivo, which may inhibit the epithelial mesenchymal transition (EMT) of tumor cells. This provides a new treatment for the control of liver cancer metastasis and recurrence.