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      GSK3β overexpression indicates poor prognosis and its inhibition reduces cell proliferation and survival of non-small cell lung cancer cells.

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          Abstract

          Glycogen synthase kinase 3 beta (GSK3β) is centrally involved in diverse cellular processes, including proliferation and apoptosis. This study aimed to investigate the influence of GSK3β expression on the prognosis of human non-small cell lung cancer (NSCLC) and the effects of GSK3β inhibition in NSCLC cell lines.

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          The glamour and gloom of glycogen synthase kinase-3.

          Richard Jope, Gail V.W. Johnson (2004)
          Glycogen synthase kinase-3 (GSK3) is now recognized as a key component of a surprisingly large number of cellular processes and diseases. Several mechanisms play a part in controlling the actions of GSK3, including phosphorylation, protein complex formation, and subcellular distribution. These are used to control and direct the far-reaching influences of GSK3 on cellular structure, growth, motility and apoptosis. Dysregulation of GSK3 is linked to several prevalent pathological conditions, such as diabetes and/or insulin resistance, and Alzheimer's disease. Therefore, much effort is currently directed towards understanding the functions and control of GSK3, and identifying methods capable of diminishing the deleterious impact of GSK3 in pathological conditions.
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            The multifaceted roles of glycogen synthase kinase 3beta in cellular signaling.

            C. A. Grimes, R Jope (2001)
            Glycogen synthase kinase-3beta (GSK3beta) is a fascinating enzyme with an astoundingly diverse number of actions in intracellular signaling systems. GSK3beta activity is regulated by serine (inhibitory) and tyrosine (stimulatory) phosphorylation, by protein complex formation, and by its intracellular localization. GSK3beta phosphorylates and thereby regulates the functions of many metabolic, signaling, and structural proteins. Notable among the signaling proteins regulated by GSK3beta are the many transcription factors, including activator protein-1, cyclic AMP response element binding protein, heat shock factor-1, nuclear factor of activated T cells, Myc, beta-catenin, CCAAT/enhancer binding protein, and NFkappaB. Lithium, the primary therapeutic agent for bipolar mood disorder, is a selective inhibitor of GSK3beta. This raises the possibility that dysregulation of GSK3beta and its inhibition by lithium may contribute to the disorder and its treatment, respectively. GSK3beta has been linked to all of the primary abnormalities associated with Alzheimer's disease. These include interactions between GSK3beta and components of the plaque-producing amyloid system, the participation of GSK3beta in phosphorylating the microtubule-binding protein tau that may contribute to the formation of neurofibrillary tangles, and interactions of GSK3beta with presenilin and other Alzheimer's disease-associated proteins. GSK3beta also regulates cell survival, as it facilitates a variety of apoptotic mechanisms, and lithium provides protection from many insults. Thus, GSK3beta has a central role regulating neuronal plasticity, gene expression, and cell survival, and may be a key component of certain psychiatric and neurodegenerative diseases.
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              Glycogen synthase kinase-3 from rabbit skeletal muscle. Separation from cyclic-AMP-dependent protein kinase and phosphorylase kinase.

              N Embi, D B Rylatt, Joshua Cohen (1980)
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                Author and article information

                Journal
                Journal ID (iso-abbrev): PLoS ONE
                Title: PloS one
                Publisher: Public Library of Science (PLoS)
                ISSN (Electronic): 1932-6203
                ISSN (Print): 1932-6203
                Publication date (Electronic): 2014
                Volume: 9
                Issue: 3
                Affiliations
                [1 ] Department of Respiratory Medicine, West China Hospital, Sichuan University, Chengdu City, Sichuan Province, China.
                [2 ] Clinical Laboratory Department, Sichuan Academy of Medical Sciences & Sichuan Provincial People's Hospital, Chengdu City, Sichuan Province, China.
                [3 ] Department of Pathology, West China Hospital, Sichuan University, West China Hospital, Sichuan University, Chengdu City, Sichuan Province, China.
                [4 ] Thoracic and Cardiovascular Surgery, West China Hospital, Sichuan University, Chengdu City, Sichuan Province, China.
                Article
                Publisher Item ID: PONE-D-13-37477
                DOI: 10.1371/journal.pone.0091231
                PMC ID: 3949982
                PubMed ID: 24618715
                SO-VID: a9bc6c0b-4eff-4ba5-bbe2-98bba7f52509
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