中晚期肝癌治疗是目前国内外研究热点，但临床一线用药索拉菲尼毒副作用较大，且预后效果差，因此亟需开发新型高效低毒药物。中药黄芩具有抑制肿瘤、提高免疫力和患者生存质量、毒性低等独特优势，给肝癌治疗带来希望。我们前期实验结果表明黄芩主要活性成分千层纸素A可显著上调肝癌细胞NAG-1基因表达及促进其编码蛋白线粒体定位，从而影响肝癌细胞增殖和转移能力，但具体机制国内外仍未见报道。本研究拟利用荧光素酶报告系统、RNA干扰、基因定点突变等技术，在NAG-1基因稳定过表达或沉默细胞株、人肝癌细胞及裸鼠移植瘤模型中，研究千层纸素A调控NAG-1基因表达机制及其与线粒体重编程的作用通路，从而阐明千层纸素A通过NAG-1基因影响线粒体功能的抗肝癌机制，为黄芩及其他“清热解毒”类中药的抗肿瘤作用提供新的理论依据，并建立以NAG-1基因调控为基础的抗肿瘤中药有效成分筛选平台。

Liver cancer prevention and treatment is one of attractive area globally since there are limited drugs available in clinic. As the first-line drug for treatment of advanced liver cancer, sorafenil has a large side effect and poor prognosis. The traditional Chinese medicine Scutellaria baicalensis Georgi (Huangqin) has been reported to suppress tumor growth, with the benefit of improving immunity and quality of life as well as low toxicity, thus shedding lights on liver cancer treatment. Our previous experimental results indicate that oroxylin A, one of active compounds derived from Huangqin, can significantly up-regulate NAG-1 gene and promote the protein mitochondrial localization, therefore affecting cell proliferation and metastasis in liver cancer cells. However, the underlying mechanisms remain obscure. In current study, we aim to investigate the mechanism by which oroxylin A regulates NAG-1 gene expression as well as the signaling pathway that NAG-1 protein targets mitochondrial reprogramming, through employing luciferase reporter system, RNA interference, site-directed gene mutation techniques, and generating NAG-1 gene expression or silence stable cell lines and isolating primary cells from human liver cancer tissues. Eventually, these studies will help to clarify the molecular mechanisms that oroxylin A suppresses liver cancer growth by NAG-1 mediated mitochondrial alteration. Our research will provide novel theoretical evidence for the anti-tumor effect of Chinese herbs like Huangqin with heat-clearing and detoxification effect, and establish a platform for screening active compounds from traditional herbs with anti-tumor effect based on NAG-1 gene regulation.