Department of Oncology, The First Affiliated Hospital of Xi'an Jiaotong University College of Medicine, Xi'an 710061, PR China.
Mol Med Rep. 2011 Jan-Feb;4(1):59-63. doi: 10.3892/mmr.2010.391. Epub 2010 Oct 27.
Resistance or insensitivity to radiation therapy is one of the hallmarks of hepatocellular carcinoma. Sensitizing radioresistant cancer by combining radiation with other therapeutics to induce apoptosis has been widely investigated. Our previous study showed that chicken anaemia virus-derived apoptin protein induced the apoptosis of hepatic carcinoma HepG2 cells. In the present study, we demonstrated that apoptin sensitizes cells to radiation-induced apoptosis using a lentivirus-apoptin expression system in hepatic carcinoma HepG2 cells. Combination therapy with radiation and apoptin dramatically induced mitochondrial cytochrome c release and the cleavage of caspases -9, -3 and -7. Our findings are also the first to show that the combination of radiation and apoptin up-regulates p53 expression. Thus, apoptin treatment represents a potential method for enhancing the effectiveness of radiotherapy in poorly responding hepatocellular carcinoma.
对放射治疗的耐药性或不敏感性是肝癌的特征之一。通过将放射治疗与其他疗法相结合以诱导细胞凋亡来使耐药性肿瘤敏感已得到广泛研究。我们之前的研究表明，鸡贫血病毒衍生的凋亡蛋白可诱导肝癌 HepG2 细胞发生凋亡。在本研究中，我们利用慢病毒-凋亡蛋白表达系统证明凋亡蛋白可使肝癌 HepG2 细胞对放射诱导的细胞凋亡敏感。放射治疗与凋亡蛋白联合治疗可显著诱导线粒体细胞色素 c 释放以及 caspase-9、-3 和 -7 的裂解。我们的研究结果也是首次表明，放射治疗与凋亡蛋白联合使用可上调 p53 表达。因此，凋亡蛋白治疗为提高低应答性肝癌放射治疗的效果提供了一种潜在方法。
