The GSK-3 kinases, GSK-3α and GSK-3β, have a central role in regulating multiple cellular processes such as glycogen synthesis, insulin signaling, cell proliferation and apoptosis. GSK-3β is the most well studied, and was originally described for its role in regulating glycogen synthase. GSK-3β has been studied as a participant in the oncogenic process in a variety of cancers due to its intersection with the PTEN/PI3K/AKT and RAS/RAF/MEK/ERK pathways. Dysregulated signaling through the Notch family of receptors can also promote oncogenesis. Normal Notch receptor signaling regulates cell fate determination in stem cell pools. GSK-3β and Notch share similar targets such β-catenin and the WNT pathway. WNT and β-catenin are involved in several oncogenic processes including those of the colon. In addition, GSK-3β may directly regulate aspects of Notch signaling. This review describes how crosstalk between GSK-3β and Notch can promote oncogenesis, using colon cancer as the primary example.

中文翻译：

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NOTCH和GSK-3信号在结肠癌和其他癌症中的相互影响。

GSK-3激酶GSK-3α和GSK-3β在调节多种细胞过程（例如糖原合成，胰岛素信号传导，细胞增殖和凋亡）中起着核心作用。GSK-3β是研究最深入的，最初因其在调节糖原合酶中的作用而被描述。由于GSK-3β与PTEN / PI3K / AKT和RAS / RAF / MEK / ERK途径相交，因此已被研究参与多种癌症的致癌过程。通过Notch受体家族的信号传导失调也可以促进肿瘤发生。正常的Notch受体信号传导调节干细胞池中细胞命运的确定。GSK-3β和Notch具有类似的靶标，例如β-catenin和WNT途径。WNT和β-catenin参与了多种致癌过程，包括结肠的致癌过程。此外，GSK-3β可以直接调节Notch信号传导的各个方面。这篇综述以结肠癌为主要例子，描述了GSK-3β与Notch之间的串扰如何促进肿瘤发生。