Cpeb3, or cytoplasmic polyadenylation element-binding protein 3, is a sequence-specific RNA-binding protein. It is involved in regulating the translation, stability, and localization of target mRNAs. Cpeb3 participates in multiple biological processes such as synaptic plasticity, learning and memory, oocyte development, and neurogenesis [2,3,5]. It also plays a role in various disease-related pathways, including those in cancer, neurodegenerative diseases, and female reproductive disorders. Genetic models, like KO/CKO mouse models, have been crucial in studying its functions.

In KO mouse models, Cpeb3 deficiency leads to various phenotypes. In female mice, it affects ovarian follicle development, causing premature ovarian insufficiency, as granulosa cell proliferation is inhibited and apoptosis increases, and the expression of Gdf9, a potential target, is decreased [6]. In conditional Cpeb3 knockout animals, neuron-specific deletion reduces inflammation-induced clinical disability in experimental autoimmune encephalomyelitis, suggesting a role in neuroinflammation [1]. In cpeb3 knockout mice, they are more susceptible to carcinogen-induced hepatocarcinogenesis and subsequent lung metastasis, as Cpeb3 suppresses hepatocellular carcinoma progression by inhibiting the translation of MTDH mRNA [4].

In conclusion, Cpeb3 is essential for multiple biological functions, including oocyte and ovarian follicle development, learning and memory, and neurogenesis. Its study using KO/CKO mouse models has provided insights into its role in diseases such as hepatocellular carcinoma, premature ovarian insufficiency, and neuroinflammatory diseases. Understanding Cpeb3 can offer new perspectives on disease mechanisms and potential therapeutic strategies.