由于未知机制，一些海洋无脊椎动物被认为不会发展肿瘤。为了初步了解肿瘤相关基因在海洋无脊椎动物发育过程中如何表达和发挥功能，我们利用海胆胚胎作为一个模型系统，对已在哺乳动物模型中被报道具有肿瘤发生基因和抑制肿瘤基因协同作用的Myc和p53/p63/p73进行了表达特征的描述。在海胆胚胎发育期间，发现p53/p63/p73复合基因在母源负载下，受精后在转录和蛋白质水平上均有下降，而Myc的转录和蛋白质在启动子表达时期进行。p53/p63/p73和Myc蛋白分别于细胞质和细胞核中存在于每个花瓣细胞中，并且在整个胚胎发育过程中保持稳定。过度表达p53/p63/p73和Myc都导致发育受损，且在囊胚阶段后存在增加的DNA损伤。p53/p63/p73增加了DNA修复/细胞死亡标志基因parp1的表达，并抑制内源中胚层基因的表达。相反，Myc不改变分化基因或癌基因的表达，但会诱导细胞形态的无序。p53/p63/p73似乎对细胞分化起着重要作用，而Myc在海胆胚胎发育过程中引起无序形态，但并非通过传统的肿瘤基因调节或凋亡通路。©2023美国解析学会。

Some marine invertebrate organisms are considered not to develop tumors due to unknown mechanisms. To gain an initial insight into how tumor-related genes may be expressed and function during marine invertebrate development, we here leverage sea urchin embryos as a model system and characterize the expressions of Myc and p53/p63/p73 which are reported to function synergistically in mammalian models as an oncogene and tumor suppressor, respectively.During sea urchin embryogenesis, a combo gene of p53/p63/p73 is found to be maternally loaded and decrease after fertilization both in transcript and protein, while Myc transcript and protein are zygotically expressed. p53/p63/p73 and Myc proteins are observed in the cytoplasm and nucleus of every blastomere, respectively, throughout embryogenesis. Both p53/p63/p73 and Myc overexpression results in compromised development with increased DNA damage after the blastula stage. p53/p63/p73 increases the expression of parp1, a DNA repair/cell death marker gene, and suppresses endomesoderm gene expressions. In contrast, Myc does not alter the expression of specification genes or oncogenes yet induces disorganized morphology.p53/p63/p73 appears to be important for controlling cell differentiation, while Myc induces disorganized morphology yet not through conventional oncogene regulations or apoptotic pathways during embryogenesis of the sea urchin.© 2023 American Association for Anatomy.