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Epithelial-Mesenchymal Transformation during Craniofacial Development

¹ Graduate Endodontics Department and
² Biomedical Sciences Department, Texas A&M University System, Baylor College of Dentistry, 3302 Gaston Ave., Dallas, TX 75266, USA;

^* corresponding author, ksvoboda{at}bcd.tamhsc.edu

Epithelial to mesenchymal phenotype transition is a common phenomenon during embryonic development, wound healing, and tumor metastasis. This transition involves cellular changes in cytoskeleton architecture and protein expression. Specifically, this highly regulated biological event plays several important roles during craniofacial development. This review focuses on the regulation of epithelial-mesenchymal transformation (EMT) during neural crest cell migration, and fusion of the secondary palate and the upper lip. Abbreviations used in this paper: BMP, bone morphogenic protein; CCFSE, 5 (and 6) carboxy 2,7' dichlorofluorescein diacetate succinimidyl ester; CNC, cranial neural crest; DiI, 1,1-dioctadecyl-3,3,3'-tetramethylindocarbocyanine perchlorate; EMT, epithelial-mesenchymal transformation; FGF, fibroblast growth factor; ILK, integrin-linked kinase; LEF1, Lymphoid enhancer factor-1; MEE, medial edge epithelia; MFS, mean fusion score; MMP, matrix metalloproteinase; PDK, 3-phosphoinostide-dependent protein kinase; Pax, paired box-1 to -9; PI-3 kinase, phosphatidylinositol-3 kinase; Ptc, patched; PTEN, phosphatase and tensin homolog deleted on chromosome ten; Shh, Sonic hedgehog; Tbx, T-box family; TGF, transforming growth factor; TIMP, tissue inhibitor of metalloproteinase.

KEY WORDS: palate • epithelial-mesenchymal transformation (EMT) • TGFß • PI-3 kinase • Akt • Smad

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