NF-kB/miR-24/miR-629在肝癌肿瘤化过程中的作用及相关分子机制研究

慢性肝炎是我国肝癌高发的主因，但慢性肝炎恶性转化（即肝癌肿瘤化）的机制仍不清楚。本课题的前期研究发现miR-24/miR-629在HCC肿瘤组织中存在异常表达，尤其是在具有慢性肝炎背景者更为明显，而NF-kB可调节miR-24/miR-629的表达，本课题将以此为线索开展如下研究：①研究与分析NF-kB、miR-24/miR-629在不同程度慢性肝炎、肝硬化、非典型增生及HCC肿瘤组织中的变化情况；②研究与分析NF-kB/miR-24/miR-629等的网络调控关系及可能的中间环节；③分析NF-kB/miR-24/miR-629在慢性肝炎恶性转化过程中的地位。通过以上研究有助阐明慢性肝炎发生恶性转化的相关机制，该项目的成功实施有助明确癌前病变到癌变过程的相关分子机制，为HCC的防治提供新的实验依据，并可能带来广泛的社会效益及经济效益。

Chronic hepatitis is the main cause of high incidence of hepatocellular carcinoma (HCC) in China, however, it is unclear how the malignant transformation of chronic hepatitis take places. Our previous studies have shown that disnormal miR-24/miR-629expression is found in the HCC tissues, especially under the chornic hepatitis conditions. Furthermore, this disnormal expression is correlated with miR-24/miR-629 expression modulated by NF-kB. Based on the aforementioned facts, we plan to investigate the following research: (1) the change of NF-kB and miR-24/miR-629, in the different-type chronic hepatitis, hepatic cirrhosis, atypical hyperplasia, and HCC tumor tissues; (2) the network of NF-kB and miR-24/miR-629, and their possible intermediate links; and (3) the role of NF-kB/miR-24/miR-629 in the malignant transformation process of chronic hepatitis. These researchs might help for us not only to elucidate the corresponding carcinogenesis of the malignant tranformation of chronic hepatitis, but to provide new experimental data about HCC prevention.