Open Access

ARTICLE

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

XIANGCAI YANG^1,2,*, YA XU³, SHUTING MEI¹, JIEJING LI^3,*

1 Department of R&D, Biotech & Science Company of UP, Guangzhou Branch, Guangzhou, 510000, China
2 State Key Laboratory of Genetic Resources and Evolution, Kunming Institute of Zoology, Chinese Academy of Sciences, Kunming, 650223, China
3 Laboratory of Developmental Disease and Natural Medicine, Medical Faculty, Kunming University of Science and Technology, Kunming, 650000, China

* Corresponding Authors:XIANGCAI YANG, ; JIEJING LI,

BIOCELL 2022, 46(2), 463-470. https://doi.org/10.32604/biocell.2021.014834

Received 03 November 2020; Accepted 23 December 2020; Issue published 20 October 2021

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.

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