癌干细胞在恶性肿瘤的复发、转移、多药耐药、不良预后中发挥重要作用并导致临床放化疗失败。阐明癌干细胞维持干性（即自我更新、分化潜能）的分子机制，将为设计新型肿瘤治疗策略、克服肿瘤的放化疗抗性、提高肿瘤临床治疗效果具有重要现实意义。肝细胞癌是我国发病率和死亡率均很高的一种恶性肿瘤，其化疗效果、预后均很差。本项目将基于我们多年对肝癌干细胞标志物鉴定、基本生物学特性、耐药特性等前期研究基础上，开展针对肝细胞癌干细胞干性维持机制的研究，具体开展以下三个方面的研究：（1）IKZF1/CD133/MINA53信号通路在肝癌干细胞增殖及干性维持中的功能；（2）IKZF1/CD133/MINA53调控肝癌干细胞干性的分子机制；（3）靶向肝癌干细胞IKZF1/CD133/MINA53信号的实验性治疗新策略。该研究成果将为靶向肝癌干细胞临床肝癌治疗方案的制订提供重要的实验依据和理论指导。

Cancer stem cells (CSC) play an important role in the recurrence, metastasis, multidrug resistance and poor prognosis of malignant tumors and lead to clinical radiotherapy and chemotherapy failure. It is of great practical significance to clarify the molecular mechanism of CSCs to maintain their stemness (ie, self-renewal and differentiation potential), which could be used to design new tumor treatment strategies, to overcome the radiotherapy and chemotherapy resistance of malignant tumors and improve the clinical effect of tumors. Hepatocellular carcinoma (HCC) is a malignant tumor with high morbidity and mortality in China. The chemotherapy effect and prognosis are very poor. Based on our previous studies on the identification of HCC CSC biomarkers, and their basic biological characteristics and drug resistance, we will focus on the study on the mechanism of stemness maintenance of HCC CSCs. The following three aspects are studied: (1) To reveal the function of IKZF1/CD133/MINA53 signaling pathway in the proliferation and dry maintenance of HCC CSCs; (2) To elucidate the molecular mechanism of IKZF1/CD133/MINA53 signaling regulating the stemness of HCC CSCs; (3) To carry out the experimental therapeutic study of targeting the KZF1/CD133/MINA53 signaling. The results of this study will provide important experimental and theoretical guidance for the developing novelty clinical treatment of targeting HCC CSCs.