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Overexpression of geranylgeranyl diphosphate synthase contributes to tumour metastasis and correlates with poor prognosis of lung adenocarcinoma

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      Abstract

      This study aimed to evaluate the biological role of geranylgeranyl diphosphate synthase ( GGPPS) in the progression of lung adenocarcinoma. GGPPS expression was detected in lung adenocarcinoma tissues by qRTPCR, tissue microarray ( TMA) and western blotting. The relationships between GGPPS expression and the clinicopathological characteristics and prognosis of lung adenocarcinoma patients were assessed. GGPPS was down‐regulated in SPCA‐1, PC9 and A549 cells using si RNA and up‐regulated in A549 cells using an adenoviral vector. The biological roles of GGPPS in cell proliferation, apoptosis, migration and invasion were determined by MTT and colony formation assays, flow cytometry, and transwell and wound‐healing assays, respectively. In addition, the regulatory roles of GGPPS on the expression of several epithelial‐mesenchymal transition ( EMT) markers were determined. Furthermore, the Rac1/Cdc42 prenylation was detected after knockdown of GGPPS in SPCA‐1 and PC9 cells. GGPPS expression was significantly increased in lung adenocarcinoma tissues compared to that in adjacent normal tissues. Overexpression of GGPPS was correlated with large tumours, high TNM stage, lymph node metastasis and poor prognosis in patients. Knockdown of GGPPS inhibited the migration and invasion of lung adenocarcinoma cells, but did not affect cell proliferation and apoptosis. Meanwhile, GGPPS inhibition significantly increased the expression of E‐cadherin and reduced the expression of N‐cadherin and vimentin in lung adenocarcinoma cells. In addition, the Rac1/Cdc42 geranylgeranylation was reduced by GGPPS knockdown. Overexpression of GGPPS correlates with poor prognosis of lung adenocarcinoma and contributes to metastasis through regulating EMT.

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      Most cited references 44

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      Each year, the American Cancer Society estimates the numbers of new cancer cases and deaths that will occur in the United States in the current year and compiles the most recent data on cancer incidence, mortality, and survival. Incidence data were collected by the National Cancer Institute (Surveillance, Epidemiology, and End Results [SEER] Program), the Centers for Disease Control and Prevention (National Program of Cancer Registries), and the North American Association of Central Cancer Registries. Mortality data were collected by the National Center for Health Statistics. In 2016, 1,685,210 new cancer cases and 595,690 cancer deaths are projected to occur in the United States. Overall cancer incidence trends (13 oldest SEER registries) are stable in women, but declining by 3.1% per year in men (from 2009-2012), much of which is because of recent rapid declines in prostate cancer diagnoses. The cancer death rate has dropped by 23% since 1991, translating to more than 1.7 million deaths averted through 2012. Despite this progress, death rates are increasing for cancers of the liver, pancreas, and uterine corpus, and cancer is now the leading cause of death in 21 states, primarily due to exceptionally large reductions in death from heart disease. Among children and adolescents (aged birth-19 years), brain cancer has surpassed leukemia as the leading cause of cancer death because of the dramatic therapeutic advances against leukemia. Accelerating progress against cancer requires both increased national investment in cancer research and the application of existing cancer control knowledge across all segments of the population.
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        The transdifferentiation of epithelial cells into motile mesenchymal cells, a process known as epithelial-mesenchymal transition (EMT), is integral in development, wound healing and stem cell behaviour, and contributes pathologically to fibrosis and cancer progression. This switch in cell differentiation and behaviour is mediated by key transcription factors, including SNAIL, zinc-finger E-box-binding (ZEB) and basic helix-loop-helix transcription factors, the functions of which are finely regulated at the transcriptional, translational and post-translational levels. The reprogramming of gene expression during EMT, as well as non-transcriptional changes, are initiated and controlled by signalling pathways that respond to extracellular cues. Among these, transforming growth factor-β (TGFβ) family signalling has a predominant role; however, the convergence of signalling pathways is essential for EMT.
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            Author and article information

            Affiliations
            [ 1 ] Department of Respiratory Medicine Jinling Hospital Southern Medical University Nanjing China
            [ 2 ] Intensive Care Unit Inner Mongolia People's Hospital Hohhot China
            [ 3 ] Center of Tumor Inner Mongolia People's Hospital Hohhot China
            Author notes
            [* ] Correspondence to: Tangfeng LV, M.D., Ph.D.

            E‐mail: bairoushui@ 123456163.com

            Yong SONG, M.D., Ph.D.

            yong_song6310@ 123456yahoo.com

            [†]

            These authors contributed equally to this work.

            Contributors
            bairoushui@163.com
            ORCID: http://orcid.org/0000-0003-4979-4131, yong_song6310@yahoo.com
            Journal
            J Cell Mol Med
            J. Cell. Mol. Med
            10.1111/(ISSN)1582-4934
            JCMM
            Journal of Cellular and Molecular Medicine
            John Wiley and Sons Inc. (Hoboken )
            1582-1838
            1582-4934
            29 January 2018
            April 2018
            : 22
            : 4 ( doiID: 10.1111/jcmm.2018.22.issue-4 )
            : 2177-2189
            29377583
            5867137
            10.1111/jcmm.13493
            JCMM13493
            © 2018 The Authors. Journal of Cellular and Molecular Medicine published by John Wiley & Sons Ltd and Foundation for Cellular and Molecular Medicine.

            This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.

            Counts
            Figures: 7, Tables: 2, Pages: 13, Words: 6521
            Product
            Funding
            Funded by: National Natural Science Foundation of China
            Award ID: 81302032
            Award ID: 81401903
            Award ID: 81572937
            Award ID: 81572273
            Funded by: Natural Science Foundation of Jiangsu province
            Award ID: BK2011658
            Award ID: BK20140736
            Funded by: Program of Nanjing Science and Technology of Nanjing Science and Technology Committee
            Award ID: 201605059
            Funded by: Jiangsu Provincial Medical Youth Talent
            Award ID: QNRC2016125
            Funded by: Inner Mongolia People's Hospital research fund
            Award ID: 2016082
            Categories
            Original Article
            Original Articles
            Custom metadata
            2.0
            jcmm13493
            April 2018
            Converter:WILEY_ML3GV2_TO_NLMPMC version:version=5.3.3 mode:remove_FC converted:25.03.2018

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