Cdyl2, short for chromodomain Y-like 2, is a gene with diverse functions. It is involved in spermatogenesis as a member of the CDY family [3,5]. It also plays roles in epigenetic regulation, as it can interact with proteins like G9a/EHMT2 and GLP/EHMT1, and regulate chromatin enrichment at specific genes [2]. Cdyl2 is associated with pathways related to cell plasticity, mitosis, and genome stability [2,4]. Understanding its functions is crucial for uncovering mechanisms in various biological processes and diseases.

In heart-related studies, circCDYL2, derived from Cdyl2, can be translated into Cdyl2-60aa. This polypeptide accelerates cardiomyocyte death after myocardial infarction by blocking APAF1 ubiquitination, suggesting its role in heart failure development [1]. In breast cancer, CDYL2 is commonly over-expressed and is positively associated with cell migration, invasion, and epithelial-to-mesenchymal transition. It epigenetically regulates MIR124, affecting NF-κB/STAT3-dependent cell plasticity [2]. In hepatocellular carcinoma, CDYL2 is down-regulated, and it inhibits cell proliferation and metastasis by modulating the SLC7A6/mTORC1/S6K pathway [3]. In breast cancer again, its four transcript variants (CDYL2a-CDYL2d) have discrete functions. CDYL2a promotes cell proliferation, while CDYL2b suppresses migration and invasion [5]. Also, CDYL2 is recruited to pericentromeres in an H3K9me3-dependent manner and is required for faithful mitosis and genome stability in breast and cervical cancer cells [4].

In conclusion, Cdyl2 has multifaceted functions in different biological processes and diseases. Studies, including those potentially using gene knockout or conditional knockout mouse models (although not explicitly detailed in references), have revealed its importance in heart failure, breast cancer, and hepatocellular carcinoma. These findings contribute to understanding disease mechanisms and potentially developing new therapeutic strategies.