EEF1D modulates proliferation and epithelial–mesenchymal transition in oral squamous cell carcinoma

Isadora Luana Flores(Universidade Estadual de Campinas (UNICAMP)), Rebeca Kawahara(Brazilian Center for Research in Energy and Materials), Márcia Cristina da Costa Miguel(Universidade Estadual de Campinas (UNICAMP)), Daniela C. Granato(Brazilian Center for Research in Energy and Materials), Romênia R. Domingues(Brazilian Center for Research in Energy and Materials), Carolina Carneiro Soares Macedo(Universidade Estadual de Campinas (UNICAMP)), Carolina Moretto Carnielli(Brazilian Center for Research in Energy and Materials), Sami Yokoo(Brazilian Center for Research in Energy and Materials), Priscila Campioni Rodrigues(Universidade Estadual de Campinas (UNICAMP)), Bárbara Vanessa de Brito Monteiro(Universidade Estadual de Campinas (UNICAMP)), Carine Ervolino de Oliveira(Universidade Estadual de Campinas (UNICAMP)), Cristiane Ribeiro Salmon(Universidade Estadual de Campinas (UNICAMP)), Francisco Humberto Nociti(Universidade Estadual de Campinas (UNICAMP)), Márcio Ajudarte Lopes(Universidade Estadual de Campinas (UNICAMP)), Alan Roger Santos‐Silva(Universidade Estadual de Campinas (UNICAMP)), Flávia Vischi Winck(Brazilian Center for Research in Energy and Materials), Ricardo D. Coletta(Universidade Estadual de Campinas (UNICAMP)), Adriana Franco Paes Leme(Brazilian Center for Research in Energy and Materials)
Clinical Science
January 29, 2016
Cited by 63Open Access
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Abstract

EEF1D (eukaryotic translation elongation factor 1δ) is a subunit of the elongation factor 1 complex of proteins that mediates the elongation process during protein synthesis via enzymatic delivery of aminoacyl-tRNAs to the ribosome. Although the functions of EEF1D in the translation process are recognized, EEF1D expression was found to be unbalanced in tumours. In the present study, we demonstrate the overexpression of EEF1D in OSCC (oral squamous cell carcinoma), and revealed that EEF1D and protein interaction partners promote the activation of cyclin D1 and vimentin proteins. EEF1D knockdown in OSCC reduced cell proliferation and induced EMT (epithelial-mesenchymal transition) phenotypes, including cell invasion. Taken together, these results define EEF1D as a critical inducer of OSCC proliferation and EMT.


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