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Abstract
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 shown to 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-like properties that largely account for immunosuppression and tumor recurrence. Therefore, identifying sensitive EMT markers may contribute to cancer prognosis and diagnosis in many facets. Previously, we showed that Elp3 plays an essential role during neural crest migration by stabilizing Snail1. In the current study, we further elucidate the molecular mechanism underlying colorectal cancer migration. We found that mElp3 exerted an identical function to xElp3 in modulating neural crest migration, and both HAT and SAM domains are imperative during this migratory process. Interestingly, overexpression of mElp3 in SW480 cells promoted cell migration and invasion, and we further showed that Elp3 stabilized Snail1 requiring integrity of both SAM and HAT domains. Our findings warrant further exploration of the specific target of Elp3 in cancer cells.
Highlights
Colorectal cancer (CRC) is a major public health issue in China and a leading cause of death worldwide (Ferlay et al, 2015)
Results mElp3 exerted an identical function to xElp3 in modulating neural crest migration It is well known that the Elongator protein 3 (Elp3) gene product is conserved range from Saccharomyces cerevisiae and Drosophila melanogaster to Caenorhabditis elegans and Arabidopsis thaliana (Wittschieben et al, 1999a)
We showed that cranial neural crest (CNC) cells of Elp3 morphants failed to emigrate from the medial region of the injected side (Figs. 1a and 1d) (Yang et al, 2016)
Summary
Colorectal cancer (CRC) is a major public health issue in China and a leading cause of death worldwide (Ferlay et al, 2015). Surgery is the mainstay of curative treatment for CRC, metastatic spread of tumor cells often occurs in refractory circumstances. Metastasis eventually causes cancer-related death in CRC cases (Ling et al, 2015). It is necessary to identify molecular targets favoring prognostics and diagnostics. Elongator protein 3 (Elp3) is the catalytic core of the Elongator complex. Together with hyperphosphorylated RNA polymerase II, it plays an essential role in transcriptional elongation (Otero et al, 1999; Wittschieben et al, 1999b; Kim et al, 2002). Elp contains an N-terminal radical S-adenosylmethionine (SAM) binding domain and a C-terminal histone acetyltransferase (HAT) domain. The HAT domain is well characterized and required for catalyzing
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