CELF6, also known as CUG-BP Elav-like family member 6, is a canonical RNA-binding protein (RBP) that plays crucial roles in post-transcriptional regulation of pre-mRNAs. It is involved in processes such as muscle-specific alternative splicing [6]. In the context of diseases, it has been associated with various cancers and neurodevelopmental disorders. Genetic models, like knockout mouse models, are valuable for studying its functions.

In cancer research, in triple-negative breast cancer (TNBC), CELF6 overexpression suppresses cell proliferation, migration, and invasion by stabilizing FBP1 mRNA, acting as a tumor suppressor [1]. In lung cancer A549 cells, increasing CELF6 expression affects the transcription and splicing of genes related to tumorigenesis, inhibiting the expression of many immune-related genes promoting tumor growth [2]. In colorectal cancer, CELF6 is downregulated and its overexpression reduces cell proliferation and stemness by modulating HOXA5 mRNA stability [3]. In cervical cancer, CELF6 overexpression suppresses HeLa cell proliferation by targeting cyclin D1 [5]. Also, in a mouse model, loss of Celf6 impairs cocaine-conditioned place preference and contextual fear conditioning, suggesting its role in conditioned learning [4].

In conclusion, CELF6 is an important RNA-binding protein with diverse functions. Through model-based research, it has been shown to play a significant role in cancer development, acting as either a tumor suppressor or being associated with cancer progression depending on the cancer type. In the nervous system, it is involved in conditioned learning. The study of CELF6 using KO mouse models has provided valuable insights into these disease-related biological processes.