Notch ligand Delta-like 1 promotes the metastasis of melanoma by enhancing tumor adhesion.

Notch ligand Delta-like 1 promotes the metastasis of melanoma by enhancing tumor adhesion.
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Notch配体Delta-like 1通过增强肿瘤粘附促进黑色素瘤转移

DOI:
10.1590/1414-431x20143368
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发表时间:
2014-04
期刊:
Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologicas
影响因子:
--
通讯作者:
Shan LQ
Shan LQ
中科院分区:
其他
文献类型:
--
作者:
Zhang JP;Li N;Bai WZ;Qiu XC;Ma BA;Zhou Y;Fan QY;Shan LQ

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Notch信号通过调节增殖、侵袭和肿瘤微环境在致瘤性和肿瘤进展中起重要作用。我们小组以前的研究表明,Notch配体Delta-like 1(Dll 1)参与黑色素瘤的血管生成,我们注意到胰蛋白酶消化表达Dll 1的B16黑色素瘤细胞比对照细胞需要更长的时间。在这篇文章中,我们扩展我们的研究,以探讨Dll 1对肿瘤细胞粘附和转移的影响。Dll 1过表达激活了B16肿瘤细胞中的Notch信号,并显著增强了B16肿瘤细胞在体外和体内的粘附能力。在小鼠肺转移模型中,B16-Dll 1细胞也具有比其对应物更高的转移潜力。沿着Dll 1表达的增加,在B16-Dll 1细胞中,N-钙粘蛋白上调,而E-钙粘蛋白未上调。这些数据表明,Notch配体Dll 1可能通过上调N-cadherin增强黑素瘤细胞的粘附和转移。
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.
主动Notch1将转化的表型赋予原代人黑色素细胞。
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