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Novel CD44-downstream signaling pathways mediating breast tumor invasion

机译:新型CD44下游信号通路介导乳腺肿瘤侵袭

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CD44, also known as homing cell adhesion molecule is a multi-structural cell molecule involved in cell-cell and cell-extracellular matrix communications. CD44 regulates a number of central signaling pathways, including PI3K/AKT, Rho GTPases and the Ras-MAPK pathways, but also acts as a growth/arrest sensor, and inhibitor of angiogenesis and invasion, in response to signals from the microenvironment. The function of CD44 has been very controversial since it acts as both, a suppressor and a promoter of tumor growth and progression. To address this discrepancy, we have previously established CD44-inducible system both in vitro and in vivo . Next, using microarray analysis, we have identified and validated Survivin, Cortactin and TGF-β2 as novel CD44-downstream target genes, and characterized their signaling pathways underpinning CD44-promoted breast cancer (BC) cell invasion. This report aims to update the literature by adding and discussing the impact of these novel three signaling pathways to better understand the CD44-signaling pathways involved in BC tumor cell invasion.
机译:CD44,也称为归巢细胞粘附分子,是涉及细胞-细胞和细胞-细胞外基质通讯的多结构细胞分子。 CD44调节许多中央信号通路,包括PI3K / AKT,Rho GTPases和Ras-MAPK通路,但也响应来自微环境的信号而充当生长/停滞传感器以及血管生成和侵袭的抑制剂。 CD44的功能一直是有争议的,因为它既是肿瘤生长和发展的抑制器又是启动子。为了解决这种差异,我们先前已经在体外和体内建立了CD44诱导系统。接下来,使用微阵列分析,我们已经鉴定并验证了Survivin,Cortactin和TGF-β2作为新的CD44下游靶基因,并表征了它们支持CD44促进的乳腺癌(BC)细胞入侵的信号通路。本报告旨在通过添加和讨论这三种新颖的信号通路的影响来更新文献,以更好地了解参与BC肿瘤细胞侵袭的CD44信号通路。

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