Glycogen Synthase Kinase-3 and phospholipase C-beta signalling: Roles and possible interactions in myelodysplastic syndromes and acute myeloid leukemia.,Biochimica et Biophysica Acta (BBA) - Molecular Cell Research

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Glycogen Synthase Kinase-3 and phospholipase C-beta signalling: Roles and possible interactions in myelodysplastic syndromes and acute myeloid leukemia.
Biochimica et Biophysica Acta (BBA) - Molecular Cell Research ( IF 4.6 ) Pub Date : 2020-01-15 , DOI: 10.1016/j.bbamcr.2020.118649
Stefano Ratti ₁ , Sara Mongiorgi ₁ , Isabella Rusciano ₁ , Lucia Manzoli ₁ , Matilde Y Follo ₁

Affiliation

GSK-3 and PLCbeta enzymes are responsible for the regulation of several signalling pathways related to many cellular functions. In hematopoietic cells, GSK-3 deficiency is correlated with an MDS-like phenotype and with leukemogenesis, showing a prognostic potential in AML cells. GSK-3 interacts with Wnt or MAPK signalling, but it is also linked to PI3K/Akt/mTOR pathways to regulate cell proliferation and apoptosis of hematopoietic stem cell progenitors. PLCbeta enzymes are involved in cell cycle progression of hematopoietic, MDS/AML and immune cells, through activation of PKC or calcium signalling. Of note, a PLCbeta1/PKCalpha pathway is modulated during MDS pathogenesis, with a specific involvement of the inositides localized in the nucleus. Here we focus on GSK-3 and PLCbeta signalling, describing the many evidences that underline the pivotal role of both GSK-3 and PLCbeta-dependent pathways in MDS/AML, their association with therapy and their possible interactions.

中文翻译：

糖原合酶激酶3和磷脂酶C-beta信号：在骨髓增生异常综合症和急性髓性白血病中的作用和可能的相互作用。

GSK-3和PLCbeta酶负责调节与许多细胞功能相关的几种信号通路。在造血细胞中，GSK-3缺乏与MDS样表型和白血病发生有关，显示出AML细胞的预后潜力。GSK-3与Wnt或MAPK信号传导相互作用，但也与PI3K / Akt / mTOR途径相关，以调节造血干细胞祖细胞的细胞增殖和凋亡。PLCbeta酶通过激活PKC或钙信号传导，参与造血，MDS / AML和免疫细胞的细胞周期进程。值得注意的是，PLCbeta1 / PKCalpha途径在MDS发病机理中受到调节，其特定参与的是细胞核中的肌苷。在这里，我们重点介绍GSK-3和PLCbeta信号，

更新日期：2020-01-15

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