Huang Fang, Ma Buyun, Wang Yigang, Xiao Ruijuan, Kong Yanping, Zhou Xiumei, Xia Dajing
1 School of Public Health, Zhejiang University , Hangzhou, China .
Cancer Biother Radiopharm. 2014 Dec;29(10):403-11. doi: 10.1089/cbr.2014.1642.
Although the treatment methods for hepatocellular carcinoma (HCC) have made a great progress on patient survival rate and life quality, the HCC recurrence still is very high. To explore the novel effective anticancer strategies for HCC, the Cancer Targeting Gene-Viro-Therapy (CTGVT) strategy was applied through oncolytic virus-delivery antitumor gene. In this article, the dual-regulated oncolytic adenovirus Ad-AFP-E1A-E1B(Δ55kDa)-Mn-SOD (briefly named AD55-Mn-SOD) was constructed using a liver cancer-specific α-fetoprotein (AFP) promoter to control replication-essential E1A gene and deliver the novel tumor suppression gene Manganese superoxide dismutase (Mn-SOD). The results indicated that the constructed AD55-Mn-SOD exerted tumor-specific features, and induced dramatic cytotoxicity in HCC cells in vitro and suppress the HCC xenografted growth in nude mice. Moreover, the anticancer mechanism of AD55-Mn-SOD is due to the activation of caspase apoptotic pathway. These data suggested that AD55-Mn-SOD could become a potential anticancer agent for liver cancer.
尽管肝细胞癌(HCC)的治疗方法在提高患者生存率和生活质量方面取得了很大进展,但HCC的复发率仍然很高。为了探索针对HCC的新型有效抗癌策略,通过溶瘤病毒递送抗肿瘤基因应用了癌症靶向基因-病毒疗法(CTGVT)策略。在本文中,使用肝癌特异性甲胎蛋白(AFP)启动子构建了双调控溶瘤腺病毒Ad-AFP-E1A-E1B(Δ55kDa)-Mn-SOD(简称为AD55-Mn-SOD),以控制复制必需的E1A基因并递送新型肿瘤抑制基因锰超氧化物歧化酶(Mn-SOD)。结果表明,构建的AD55-Mn-SOD具有肿瘤特异性特征,在体外对HCC细胞诱导了显著的细胞毒性,并抑制了裸鼠体内HCC异种移植瘤的生长。此外,AD55-Mn-SOD的抗癌机制是由于激活了半胱天冬酶凋亡途径。这些数据表明,AD55-Mn-SOD可能成为一种潜在的肝癌抗癌药物。