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Endocytosis and serpentine filopodia drive blebbishield-mediated resurrection of apoptotic cancer stem cells.
Cell Death Discovery ( IF 7 ) Pub Date : 2016-05-27 , DOI: 10.1038/cddiscovery.2015.69
Goodwin G Jinesh 1 , Ashish M Kamat 1
Affiliation  

The blebbishield emergency program helps to resurrect apoptotic cancer stem cells (CSCs) themselves. Understanding the mechanisms behind this program is essential to block resurrection of CSCs during cancer therapy. Here we demonstrate that endocytosis drives serpentine filopodia to construct blebbishields from apoptotic bodies and that a VEGF-VEGFR2-endocytosis-p70S6K axis governs subsequent transformation. Disengagement of RalGDS from E-cadherin initiates endocytosis of RalGDS and its novel interaction partners cdc42, VEGFR2, cleaved β-catenin, and PKC-ζ as well as its known interaction partner K-Ras. We also report novel interactions of p45S6K (cleaved p70S6K) and PKM-ζ with PAK-1 filopodia-forming machinery specifically in blebbishields. Thus, a RalGDS-endocytosis-filopodia-VEGFR2-K-Ras-p70S6K axis drives the blebbishield emergency program, and therapeutic targeting of this axis might prevent resurrection of CSCs during cancer therapy.

中文翻译:

内吞作用和蛇形丝状伪足驱动凋亡双歧杆菌介导的凋亡性癌症干细胞的复活。

blebbishield应急计划有助于使凋亡的癌症干细胞(CSC)自身复活。了解该程序背后的机制对于阻止CSC在癌症治疗期间的复活至关重要。在这里,我们证明内吞作用驱动蛇形丝状伪足从凋亡小体构建起起泡盾,并且VEGF-VEGFR2-内吞作用-p70S6K轴控制后续转化。RalGDS从E-钙粘着蛋白上脱离会启动RalGDS及其新的相互作用伴侣cdc42,VEGFR2,裂解的β-catenin和PKC-ζ及其已知的相互作用伴侣K-Ras的内吞作用。我们还报告了p45S6K(裂解的p70S6K)和PKM-ζ与PAK-1丝状伪足形成机器的新型相互作用,特别是在blebbishields中。因此,RalGDS-吞噬作用-丝虫-VEGFR2-K-Ras-p70S6K轴可驱动blebbishield应急程序,
更新日期:2019-11-01
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