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Sam68 Allows Selective Targeting of Human Cancer Stem Cells
Cell Chemical Biology ( IF 8.6 ) Pub Date : 2017-06-22 , DOI: 10.1016/j.chembiol.2017.05.026
Yannick D. Benoit , Ryan R. Mitchell , Ruth M. Risueño , Luca Orlando , Borko Tanasijevic , Allison L. Boyd , Lili Aslostovar , Kyle R. Salci , Zoya Shapovalova , Jennifer Russell , Masakatsu Eguchi , Diana Golubeva , Monica Graham , Anargyros Xenocostas , Michael R. Trus , Ronan Foley , Brian Leber , Tony J. Collins , Mickie Bhatia

Targeting of human cancer stem cells (CSCs) requires the identification of vulnerabilities unique to CSCs versus healthy resident stem cells (SCs). Unfortunately, dysregulated pathways that support transformed CSCs, such as Wnt/β-catenin signaling, are also critical regulators of healthy SCs. Using the ICG-001 and CWP family of small molecules, we reveal Sam68 as a previously unappreciated modulator of Wnt/β-catenin signaling within CSCs. Disruption of CBP-β-catenin interaction via ICG-001/CWP induces the formation of a Sam68-CBP complex in CSCs that alters Wnt signaling toward apoptosis and differentiation induction. Our study identifies Sam68 as a regulator of human CSC vulnerability.

中文翻译:

Sam68允许选择性靶向人类癌症干细胞

靶向人类癌症干细胞(CSC)需要确定CSC与健康的常驻干细胞(SC)相比特有的漏洞。不幸的是,支持转化的CSC的失调途径,例如Wnt /β-catenin信号传导,也是健康SC的关键调节因子。使用ICG-001和CWP小分子家族,我们揭示了Sam68是CSC中Wnt /β-catenin信号传导以前未被认识的调节剂。通过ICG-001 / CWP破坏CBP-β-catenin相互作用会诱导CSC中Sam68-CBP复合物的形成,从而改变Wnt信号通路朝凋亡和分化诱导的方向。我们的研究确定Sam68是人类CSC脆弱性的调节因子。
更新日期:2017-07-22
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