Regulation of epithelial–mesenchymal transition in endometrial cancer: connecting PI3K, estrogen signaling, and microRNAs

• C. N. Kent ^[1] ; I. K. Guttilla Reed ^[1]
  1. [1] University of Saint Joseph

     University of Saint Joseph

     RAE de Macao (China)

     
• Localización: Clinical & translational oncology, ISSN 1699-048X, Vol. 18, Nº. 11 (November 2016), 2016, págs. 1056-1061
• Idioma: inglés
• Texto completo no disponible (Saber más ...)
• Resumen

  • Endometrial cancer (EC) prognosis is dependent on many factors such as time of diagnosis, histological type, and degree of invasion. Type I EC has a more favorable prognosis as it is less prone to myometrial invasion, which is believed to be the first step in the metastatic cascade. Type II EC displays a more aggressive and motile phenotype, and therefore has a poorer prognosis. Recent work suggests that despite the epithelial nature of Type I and Type II endometrial tumors, both are capable of undergoing an epithelial–mesenchymal transition (EMT), which may facilitate myometrial invasion and metastasis. Activation of the PI3K/Akt pathway has been shown to contribute to EMT through the upregulation of EMT-associated factors. Recent research has also linked estrogen signaling and microRNAs to the regulatory mechanisms that drive EMT in EC. Understanding the intricate relationships between these pathways will provide a better understanding of metastatic progression in EC.