RESUMEN

Notch signaling plays a vital role in tumorigenicity and tumor progression by regulating proliferation, invasion, and the tumor microenvironment. Previous research by our group indicated that Notch ligand Delta-like 1 (Dll1) is involved in angiogenesis in melanoma, and we noticed that it took a longer time to trypsinize Dll1-expressing B16 melanoma cells than the control cells. In this article, we extended our study to investigate the effects of Dll1 on tumor cell adhesion and metastasis. Dll1 overexpression activated Notch signaling in B16 tumor cells and significantly enhanced the adhering capacity of B16 tumor cells both in vitro and in vivo. B16-Dll1 cells also had a higher metastatic potential than their counterpart in the mouse model of lung metastasis. Along with increased Dll1 expression, N-cadherin, but not E-cadherin, was upregulated in B16-Dll1 cells. These data suggested that Notch ligand Dll1 may enhance the adhesion and metastasis of melanoma cells by upregulation of N-cadherin.

Asunto(s)

Animales , Cadherinas/biosíntesis , Péptidos y Proteínas de Señalización Intercelular/metabolismo , Neoplasias Pulmonares/secundario , Melanoma Experimental/secundario , Proteínas de la Membrana/metabolismo , Transducción de Señal/genética , Western Blotting , Adhesión Celular , Técnicas de Cultivo de Célula , Línea Celular Tumoral , Expresión Génica , Proteínas Fluorescentes Verdes , Células Endoteliales de la Vena Umbilical Humana/fisiología , Melanoma Experimental/patología , Reacción en Cadena en Tiempo Real de la Polimerasa , Regulación hacia Arriba