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CD271/p75在神经嵴衍生的黑色素瘤可塑性中的趋同作用。

The convergent roles of CD271/p75 in neural crest-derived melanoma plasticity.

作者信息

Kasemeier-Kulesa Jennifer C, Kulesa Paul M

机构信息

Stowers Institute for Medical Research, Kansas City, MO 64110, USA.

Stowers Institute for Medical Research, Kansas City, MO 64110, USA; Department of Anatomy and Cell Biology, University of Kansas Medical Center, Kansas City, KS 66160, USA.

出版信息

Dev Biol. 2018 Dec 1;444 Suppl 1(Suppl 1):S352-S355. doi: 10.1016/j.ydbio.2018.04.008. Epub 2018 Apr 13.

Abstract

The embryonic microenvironment is an important source of signals that promote multipotent cells to adopt a specific fate and direct cells along distinct migratory pathways. Yet, the ability of the embryonic microenvironment to retain multipotent progenitors or reprogram de-differentiated cells is less clear. Mistakes in cell differentiation or migration often result in developmental defects and tumorigenesis, including aggressive cancers that share many characteristics with embryonic progenitor cells. This is a striking feature of the vertebrate neural crest, a multipotent and highly migratory cell population first identified by His (1868) with the potential to metamorphose into aggressive melanoma cancer. In this perspective, we address the roles of CD271/p75 in tumor initiation, phenotype switching and reprogramming of metastatic melanoma and discuss the convergence of these roles in melanoma plasticity.

摘要

胚胎微环境是促进多能细胞确定特定命运并引导细胞沿着不同迁移途径的重要信号来源。然而,胚胎微环境保留多能祖细胞或重编程去分化细胞的能力尚不清楚。细胞分化或迁移中的错误通常会导致发育缺陷和肿瘤发生,包括与胚胎祖细胞具有许多共同特征的侵袭性癌症。这是脊椎动物神经嵴的一个显著特征,神经嵴是His(1868年)首次发现的多能且高度迁移的细胞群体,具有转变为侵袭性黑色素瘤的潜力。从这个角度出发,我们探讨了CD271/p75在转移性黑色素瘤的肿瘤起始、表型转换和重编程中的作用,并讨论了这些作用在黑色素瘤可塑性中的趋同性。

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