ZMYM1, zinc finger MYM-type containing 1, may be involved in multiple biological processes. It has been associated with pathways related to neuronal differentiation, epithelial-mesenchymal transition (EMT), and potentially in processes related to smooth muscle cell phenotypic transitions, preadipocyte differentiation, and more. Its study in genetic models could potentially provide insights into its functions in normal and disease-related biological contexts [2,3,5].

In gastric cancer, METTL3-mediated m6A modification of ZMYM1 mRNA enhances its stability via the HuR-dependent pathway. ZMYM1 then binds to and mediates the repression of the E-cadherin promoter by recruiting the CtBP/LSD1/CoREST complex, facilitating the EMT program and metastasis. In liver hepatocellular carcinoma, the METTL3-m6A-ZMYM1 axis may accelerate metastasis through inactivation of the RAS/ERK/c-FOS pathway and changes in E-cadherin, N-cadherin, and Vimentin expressions [1,4]. In neuroblastoma, dysregulation of ZMYM1 may lead to malignant transformation by affecting early and late stages of normal neuronal differentiation [2].

In conclusion, ZMYM1 plays essential roles in processes like EMT and neuronal differentiation, with implications in cancer metastasis and neuroblastoma pathogenesis. The study of ZMYM1 in relevant genetic models has contributed to understanding its role in these disease areas, highlighting its potential as a therapeutic target in anti-metastatic strategies against gastric and liver cancers and in understanding neuroblastoma development [1,2,4].