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盐酸阿霉素(DOX)作为一种抗肿瘤抗生素,通过抑制癌细胞遗传物质的合成,对多种肿瘤均有杀伤作用,然而,其单独作用疗效有限,且加大剂量时其副作用较强。目前,携带抗癌基因的溶瘤腺病毒在肿瘤治疗中的作用日渐显现,溶瘤腺病毒ZD55-Trail联合DOX治疗肝癌的研究鲜有报道。通过MTT和结晶紫染色试验检测DOX药物处理对肝癌细胞系Bel-7404存活率的变化情况;Hoechst33342染色和流式细胞术检测肝癌细胞的凋亡;Western blot检测Trail蛋白和凋亡相关蛋白的表达;免疫荧光和流式细胞术检测凋亡相关受体表达的情况。结果显示,ZD55-Trail与DOX联合使用能够有效抑制肝癌细胞增长并诱导其凋亡,并且联合处理能增加Trail受体DR4和DR5的表达。初步探讨了DOX与ZD55-Trail两者协同诱导肝癌细胞凋亡的机制,为利用ZD55-Trail与DOX联合治疗肝癌提供依据。
Doxorubicin hydrochloride (DOX), as an antitumor antibiotic, can kill many kinds of tumors by inhibiting the synthesis of genetic material of cancer cells. However, DOX alone has a limited curative effect and its side effect is strong when the dose is increased. At present, the role of oncolytic adenovirus carrying anti-oncogene in tumor therapy is increasingly apparent. The study of oncolytic adenovirus ZD55-Trail combined with DOX in the treatment of liver cancer has rarely been reported. The survival rate of Bel-7404 cells treated with DOX was measured by MTT and crystal violet staining. The apoptosis of hepatocellular carcinoma cells was detected by Hoechst33342 staining and flow cytometry. The expressions of Trail protein and apoptosis-related protein were detected by Western blot Immunofluorescence and flow cytometry were used to detect the expression of apoptosis related receptors. The results showed that the combination of ZD55-Trail and DOX can effectively inhibit the growth of hepatocellular carcinoma cells and induce their apoptosis, and the combined treatment can increase the expression of Trail receptor DR4 and DR5. The mechanism of DOX and ZD55-Trail synergistically inducing apoptosis in hepatocellular carcinoma cells was preliminarily discussed, which provided the basis for the combination of ZD55-Trail and DOX in the treatment of hepatocellular carcinoma.