Genomic instability underlies genesis and the development of various types of cancer. During tumorigenesis, cancer initiating cells assume a set of features, which allow them to survive and proliferate. Different mutations and chromosomal alterations promote a selection of the most aggressive cancer clones that worsen the prognosis of the disease. Despite that caspase-2 was described as a protease fulfilling an initiator and an effector function in apoptosis, it has recently been discovered to play an important role in the maintenance of genomic integrity and normal chromosome configuration. This protein is able to stabilize p53 and affect the level of transcription factors, which activates cell response to oxidative stress. Here we focus on the discussion on the mechanism(s) of how caspase-2 regulates genomic stability and decreases tumorigenesis.

基因组不稳定性是各种癌症发生和发展的基础。在肿瘤发生过程中，癌症起始细胞具有一组特征，使它们能够存活和增殖。不同的突变和染色体改变促进选择最具侵袭性的癌症克隆，从而使疾病的预后恶化。尽管 caspase-2 被描述为在细胞凋亡中发挥引发剂和效应子功能的蛋白酶，但最近发现它在维持基因组完整性和正常染色体构型方面发挥重要作用。这种蛋白质能够稳定 p53 并影响转录因子的水平，从而激活细胞对氧化应激的反应。在这里，我们重点讨论 caspase-2 如何调节基因组稳定性和减少肿瘤发生的机制。