Pathways that were enriched by the differentially expressed genes downstream of one or more of the causal splicing events include neural developmental pathways such as neurogenesis and gliogenesis, as well as neuropathological pathways such as Parkinson’s and Alzheimer’s diseases. Interestingly, each of the causal splicing events implicated the epithelial-mesenchymal transition (EMT) pathway, which underlies many fundamental biological processes, including neural tube formation and cancer metastasis [74]. The host gene LINC00665 is known to regulate EMT in cancer [71], and alcohol stimulates the EMT program in cancer cells, which leads to cancer progression [75]. These data further support the overlap of AUD with neurodegenerative disease [76], as well as a role of splicing in the development of alcohol-related cancers.
