| Summary: | 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.
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