抑癌基因P53通过与其结合蛋白ASP家族的成员相互作用而对众多肿瘤的形成具有重要影响，这一领域也是目前肿瘤学研究的热点之一。ASPP2可通过P53依赖或P53依赖途径诱导细胞凋亡，从而抑制肿瘤的形成和发展。然而，最近我们通过5'RACE技术发现了一种新的、被截短的、含有880个氨基酸的ASPP2异构体（ΔASPP2）。初步研究显示ΔASPP2不仅能抑制细胞凋亡，也能抑制细胞自噬，而自噬能明显地影响肿瘤的发生和生存。同时在临床肝癌标本中也发现△ASPP2表达显著增高。然而△ASPP2对ASPP2介导的P53依赖或非P53依赖途径细胞凋亡的机制和对肝癌发生的影响却是空白。本研究将通过ΔASPP2肝组织特异表达小鼠模型，利用分子生物学和细胞生物学技术，探究ASPP2和ΔASPP2表达失衡在肝癌形成和发展中的作用，从而探索肝癌形成新的分子机制，并为寻找肝癌生物治疗靶位提供新的线索。

P53, a tumor suppressor gene, can bind to ASPP family members and play a critical role in tumor development. This field has been one of the hot spots for cancer research. ASPP2 can induce apoptosis through p53 dependent and independent pathways, which suppresses tumor development and even tumor growth. However, a recent study had identified ΔASPP2, which is an isoform of ASPP2 and contains 880 amino acid residues shorter than ASPP2 at N terminal. Preliminary studies have shown that ΔASPP2 can inhibit not only apoptosis, but also autophagy which can significantly affect tumor development and survival. Furthermore, the level of ΔASPP2 was identified to be higher in tissues of hepatocellular carcinoma (HCC). However, it is still unknown that how ΔASPP2 regulate ASPP2 mediated apoptosis by p53-dependent and -independent pathways and how ΔASPP2 affects HCC development. This study will use mice characterised by specific ΔASPP2 expression in liver tissue, molecular biology and cell biology techniques, to study the effects of the imbalance between ASPP2 andΔASPP2 expression on HCC development. This can give us new ideas about molecular mechanisms on HCC development and provide us new targets on curing HCC.