Glycogen synthetase kinase-3 (GSK-3) and microRNAs (miRs) affect many critical signaling pathways important in cell growth. GSK-3 is a serine/threonine (S/T) protein kinase. Often when GSK-3 phosphorylates other proteins, they are inactivated and the signaling pathway is shut down. The PI3K/PTEN/AKT/GSK3/mTORC1 pathway plays key roles in regulation of cell growth, apoptosis, drug resistance, malignant transformation and metastasis and is often deregulated in cancer. When GSK-3 is phosphorylated by AKT it is inactivated and this often leads to growth promotion. When GSK-3 is not phosphorylated by AKT or other kinases at specific negative-regulatory residues, it can modify the activity of many proteins by phosphorylation, some of these proteins promote while others inhibit cell proliferation. This is part of the conundrum regarding GSK-3. The central theme of this review is the ability of GSK-3 to serve as either a tumor suppressor or a tumor promoter in cancer which is likely due to its diverse protein substrates. The effects of multiple miRs which bind mRNAs encoding GSK-3 and other signaling molecules and how they affect cell growth and sensitivity to various therapeutics will be discussed as they serve to regulate GSK-3 and other proteins important in controlling proliferation.

糖原合成酶激酶3（GSK-3）和微小RNA（miRs）影响细胞生长中重要的许多关键信号通路。GSK-3是一种丝氨酸/苏氨酸（S / T）蛋白激酶。通常，当GSK-3磷酸化其他蛋白质时，它们会失活，信号传导途径会关闭。PI3K / PTEN / AKT / GSK3 / mTORC1通路在调节细胞生长，凋亡，耐药性，恶性转化和转移中起关键作用，并且在癌症中常常被放松调节。当GSK-3被AKT磷酸化时，它会失活，这通常会促进生长。当GSK-3未在特定的负调控残基处被AKT或其他激酶磷酸化时，它可以通过磷酸化来修饰许多蛋白质的活性，其中一些蛋白质促进而其他蛋白质则抑制细胞增殖。这是有关GSK-3难题的一部分。这篇综述的中心主题是GSK-3充当癌症中肿瘤抑制因子或肿瘤启动子的能力，这可能是由于其多种蛋白质底物所致。由于它们结合调节GSK-3和其他对控制增殖至关重要的蛋白质，因此将讨论与编码GSK-3和其他信号分子的mRNA结合的多个miR的作用，以及它们如何影响细胞生长以及对各种疗法的敏感性。