Cpeb2, cytoplasmic polyadenylate element-binding protein 2, is an RNA-binding protein that plays crucial roles in multiple biological processes. It is involved in translational regulation, which impacts various cellular functions, and is associated with pathways related to cell proliferation, apoptosis, and differentiation. Genetic models, such as knockout (KO) mouse models, have been instrumental in studying its functions [1-9].

In glioma, Cpeb2 is downregulated and its overexpression inhibits cell proliferation and promotes apoptosis by increasing p21 mRNA stability and inducing G1 cell-cycle arrest [1]. In brown adipocytes, Cpeb2-KO mice show impaired thermogenesis and obesogenic phenotypes as Cpeb2-activated Prdm16 translation is critical for brown adipocyte function [2]. In preeclampsia, Cpeb2 is lowly expressed, and its upregulation promotes trophoblast cell functions by inhibiting SSTR3 translation through polyadenylation [3]. In multiple myeloma, Cpeb2 is upregulated, and its downregulation reduces cell proliferation and angiogenesis [4]. In renal cancer, Cpeb2 is upregulated and promotes cell proliferation and migration via a negative feedback loop with p53 [5].

In conclusion, Cpeb2 has diverse functions in different biological contexts. Model-based research, especially KO mouse models, has revealed its significance in diseases like glioma, obesity, preeclampsia, multiple myeloma, and renal cancer. These findings highlight Cpeb2 as a potential biomarker and therapeutic target in various disease areas.