Development of new IFN-strategy that based on DNA repair mechanism

本研究旨在阐明ifn - β对肝细胞癌（HCC）发生的预防作用的分子机制，建立肝癌的化学预防策略。我们发现p21的异常表达，是一种已知的细胞周期蛋白依赖性激酶（CDK）抑制剂，是肝癌发生及其预防的关键机制。ifn - β将细胞质中致癌的p21转移至细胞核，使其发挥原有的抗增殖功能。我们可以探索ifn - β的这种抗癌机制，以便应用于临床研究。

The aim of this study is to clarify the molecular mechanisms of preventive effect of IFN-beta for the occurrence of hepatocellular carcinoma (HCC) and to establish the strategy of chemoprevention of HCC. We found that aberrant expression of p21, that was a known cyclin-dependent kinase (CDK) inhibitor, was a key mechanism for hepatocarcinogenesis and it’s prevention. IFN-beta shifted cytoplasmic p21, which was oncogenic, to nucleus, making them to exert original anti-proliferative function. We may explore this anti-cancer mechanism of IFN-beta in order to apply to clinical studies.