Elp3 modulates neural crest and colorectal cancer migration requiring functional integrity of HAT and SAM domains

Cell migration is a finely tuned biological process that often involves epithelial-mesenchymal transition (EMT).EMT is typically characterized by the upregulation of mesenchymal markers such as Snail1. This process has been shownto be of critical importance to normal developmental processes, including neural crest migration and invasion.Interestingly, similar mechanisms are utilized in disease processes, such as tumor metastasis and migration. Notably,EMT and EMT-like processes confer tumor cells with the ability to migrate, invade, and adopt stem cell-likeproperties that largely account for immunosuppression and tumor recurrence. Therefore, identifying sensitive EMTmarkers may contribute to cancer prognosis and diagnosis in many facets. Previously, we showed that Elp3 plays anessential role during neural crest migration by stabilizing Snail1. In the current study, we further elucidate themolecular mechanism underlying colorectal cancer migration. We found that mElp3 exerted an identical function toxElp3 in modulating neural crest migration, and both HAT and SAM domains are imperative during this migratoryprocess. Interestingly, overexpression of mElp3 in SW480 cells promoted cell migration and invasion, and we furthershowed that Elp3 stabilized Snail1 requiring integrity of both SAM and HAT domains. Our findings warrant furtherexploration of the specific target of Elp3 in cancer cells.