CELF6, also known as CUG-BP Elav-like family member 6, is an RNA-binding protein. It plays crucial roles in post-transcriptional regulation of pre-mRNAs, including modulating alternative splicing and mRNA stability. It is involved in pathways related to cell proliferation, tumorigenesis, and conditioned learning, and is thus of great biological importance. Genetic models, such as mouse models, have been valuable in studying its functions [1,2,3,4,5,6,7,8,9,10].

In cancer research, CELF6 shows tumor-suppressive effects in multiple cancer types. In triple-negative breast cancer, overexpression of CELF6 suppresses cell proliferation, migration, and invasion by stabilizing FBP1 mRNA [1]. In lung cancer, increasing CELF6 in A549 cells affects the transcription and splicing of genes related to tumorigenesis, inhibiting the expression of many immune-related genes promoting tumorigenesis [2]. In colorectal cancer, overexpression of CELF6 reduces cell proliferation and stemness by modulating HOXA5 mRNA stability [4]. In cervical cancer, CELF6 overexpression suppresses HeLa cell proliferation by affecting cyclin D1 protein stability [6]. In contrast, in some cases like the role of lncRNA LINC01594 in colorectal cancer, it promotes metastasis by inhibiting CELF6-mediated splicing of oncogenic CD44 variants [7]. In the nervous system, Celf6 mutant mice show impaired conditioned learning, indicating its importance in this process [5].

In conclusion, CELF6 is an important RNA-binding protein that regulates various biological processes. Its role in cancer as a potential tumor suppressor and its function in the nervous system for conditioned learning are well-demonstrated through model-based research. Mouse models, especially those with Celf6 knockout or knockdown, have been instrumental in revealing these functions, providing insights into cancer biology and neurodevelopmental-related diseases [1,2,3,4,5,6,7,10].