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      PTEN/AKT upregulation of TMSB10 contributes to lung cancer cell growth and predicts poor survival of the patients

      1 , 2 , 3 , 4 , 5 , 6
      Bioscience, Biotechnology, and Biochemistry
      Oxford University Press (OUP)

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          ABSTRACT

          PTEN/AKT signaling cascade is frequently activated in various cancers, including lung cancer. The downstream effector of this signaling cascade is poorly understood. β-Thymosin 10 (TMSB10) functions as an oncogene or tumor suppressors in cancers, whereas its significance in lung cancer remains unknown. In this study, we showed that the activation of PTEN/AKT signaling promoted the expression of TMSB10. Based on the TCGA database, TMSB10 was upregulated in lung cancer tissues and its overexpression was correlated with poor prognosis of lung cancer patients. Functional experiments demonstrated that TMSB10 knockdown suppressed, while its overexpression promoted the proliferation, growth, and migration of lung cancer cells. Apoptosis and epithelial-mesenchymal transition were also regulated by TMSB10. We therefore suggest that TMSB10 is a novel oncogene for lung cancer. Targeting TMSB10 may benefit lung cancer patients with activated PTEN/AKT signaling.

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          AKT/PKB signaling: navigating downstream.

          The serine/threonine kinase Akt, also known as protein kinase B (PKB), is a central node in cell signaling downstream of growth factors, cytokines, and other cellular stimuli. Aberrant loss or gain of Akt activation underlies the pathophysiological properties of a variety of complex diseases, including type-2 diabetes and cancer. Here, we review the molecular properties of Akt and the approaches used to characterize its true cellular targets. In addition, we discuss those Akt substrates that are most likely to contribute to the diverse cellular roles of Akt, which include cell survival, growth, proliferation, angiogenesis, metabolism, and migration.
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            Non-small-cell lung cancers: a heterogeneous set of diseases.

            Non-small-cell lung cancers (NSCLCs), the most common lung cancers, are known to have diverse pathological features. During the past decade, in-depth analyses of lung cancer genomes and signalling pathways have further defined NSCLCs as a group of distinct diseases with genetic and cellular heterogeneity. Consequently, an impressive list of potential therapeutic targets was unveiled, drastically altering the clinical evaluation and treatment of patients. Many targeted therapies have been developed with compelling clinical proofs of concept; however, treatment responses are typically short-lived. Further studies of the tumour microenvironment have uncovered new possible avenues to control this deadly disease, including immunotherapy.
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              Genomic landscape of lung adenocarcinoma in East Asians

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                Author and article information

                Journal
                Bioscience, Biotechnology, and Biochemistry
                Oxford University Press (OUP)
                1347-6947
                April 2021
                March 24 2021
                December 29 2020
                April 2021
                March 24 2021
                December 29 2020
                : 85
                : 4
                : 805-813
                Affiliations
                [1 ]Department of Lymphadenopathy
                [2 ]Department of Thoracic Surgery, Hebei General Hospital
                [3 ]Department of Pharmacology, Hebei Medical University, Shijiazhuang, Hebei, P.R. China
                [4 ]Department of Thoracic Surgery, Fourth Hospital of Hebei Medical University, Hebei, P. R. China
                [5 ]Department of Laboratory, Baotou Cancer Hospital, Baotou, Inner Mongolia, P.R. China
                [6 ]Department of Oncology, Fourth Hospital of Hebei Medical University, Hebei, P. R. China
                Article
                10.1093/bbb/zbaa113
                33686397
                1f46292f-d2e6-4b0c-b1a0-68fda3892dfb
                © 2020

                https://academic.oup.com/journals/pages/open_access/funder_policies/chorus/standard_publication_model

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