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      OncoTargets and Therapy (submit here)

      This international, peer-reviewed Open Access journal by Dove Medical Press focuses on the pathological basis of cancers, potential targets for therapy and treatment protocols to improve the management of cancer patients. Publishing high-quality, original research on molecular aspects of cancer, including the molecular diagnosis, since 2008. Sign up for email alerts here. 50,877 Monthly downloads/views I 4.345 Impact Factor I 7.0 CiteScore I 0.81 Source Normalized Impact per Paper (SNIP) I 0.811 Scimago Journal & Country Rank (SJR)

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      Knockdown of SLC35F2 Inhibits the Proliferation and Metastasis of Bladder Cancer Cells

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          Abstract

          Background

          Many studies have shown that solute carrier family 35 member F2 (SLC35F2) plays a key role in the biological processes of multiple cancers. However, there have been no reports on the role of SLC35F2 in the occurrence and development of bladder cancer (BC).

          Methods

          SLC35F2 expression data and clinical and prognostic information from BC patients were obtained from databases. SLC35F2 expression in BC was verified by quantitative real-time PCR (qRT-PCR). The influence of SLC35F2 knockdown on the proliferation, apoptosis, migration and invasion in the 5637 and T24 cell lines was studied, and tumor formation experiments were performed in nude mice. Gene set enrichment analysis (GSEA) was used to predict the pathways and functions of SLC35F2 in BC.

          Results

          SLC35F2 was highly expressed in BC tissues and was associated with invasiveness and T stage in BC patients. SLC35F2 knockdown can inhibit the proliferation, migration and invasion of BC cells and can promote apoptosis. SLC35F2 knockdown significantly reduced tumorigenesis in nude mice. GSEA showed that BC, pathways in cancer, apoptosis and the P53 signaling pathway were significantly enriched in SLC35F2 high expression phenotype.

          Conclusion

          SLC35F2 can promote malignant progression and is a potential therapeutic target in BC.

          Most cited references31

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          International variations in bladder cancer incidence and mortality.

          Previous studies have reported substantial worldwide regional variations in bladder cancer (BCa) incidence and mortality. To describe contemporary international variations in BCa incidence and mortality rates and trends using the most recent data from the International Agency for Research on Cancer (IARC). Estimated 2008 BCa incidence and mortality rates for each country by sex were obtained from GLOBOCAN. Recent trends in incidence for 43 countries and in mortality for 64 countries were assessed by join-point model using data from the IARC's Cancer Incidence in Five Continents and from the World Health Organisation's mortality database, respectively. The highest incidence rates for both men and women are found in Europe, the United States, and Egypt, and the lowest rates are found in sub-Saharan Africa, Asia, and South America. Mortality rates are highest in parts of Europe and northern Africa and lowest in Asia, Central America, and middle Africa. Incidence rates among men decreased in 11 of 43 countries (46 registries) (North America, western and northern Europe), remained stable in 20, and increased in 12 countries (southern, central, and eastern Europe). Among women, incidence rates decreased in 10 countries, stabilised in 22 countries, and increased in 12 countries. Mortality rates among men decreased in 32 of 65 countries (throughout all world regions except Central and South America), stabilised in 30 countries, and increased in 3 (Romania, Slovenia, and Cuba). Among women, mortality rates decreased in 24 countries, remained stable in 36 countries, and increased in 5 countries (central and eastern Europe). Incidence and mortality rates in general decreased in most Western countries but increased in some eastern European and developing countries. These patterns in part may reflect differences in the stage and extent of the tobacco epidemic, changes in coding practices, prevalence of schistosomiasis (Africa), and occupational exposure. Copyright © 2013 European Association of Urology. Published by Elsevier B.V. All rights reserved.
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            Analysis and update of the human solute carrier (SLC) gene superfamily

            The solute-carrier gene (SLC) superfamily encodes membrane-bound transporters. The SLC superfamily comprises 55 gene families having at least 362 putatively functional protein-coding genes. The gene products include passive transporters, symporters and antiporters, located in all cellular and organelle membranes, except, perhaps, the nuclear membrane. Transport substrates include amino acids and oligopeptides, glucose and other sugars, inorganic cations and anions (H+, HCO3 -, Cl-, Na+, K+, Ca2+, Mg2+, PO4 3-, HPO4 2-, H2PO4 -, SO4 2-, C2O4 2-, OH-,CO3 2-), bile salts, carboxylate and other organic anions, acetyl coenzyme A, essential metals, biogenic amines, neurotransmitters, vitamins, fatty acids and lipids, nucleosides, ammonium, choline, thyroid hormone and urea. Contrary to gene nomenclature commonly assigned on the basis of evolutionary divergence http://www.genenames.org/, the SLC gene superfamily has been named based largely on transporter function by proteins having multiple transmembrane domains. Whereas all the transporters exist for endogenous substrates, it is likely that drugs, non-essential metals and many other environmental toxicants are able to 'hitch-hike' on one or another of these transporters, thereby enabling these moieties to enter (or leave) the cell. Understanding and characterising the functions of these transporters is relevant to medicine, genetics, developmental biology, pharmacology and cancer chemotherapy.
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              New insights into cyclins, CDKs, and cell cycle control.

              Since their initial discovery in yeast, cyclin-dependent kinases have proven to be universal regulators of the cell cycle in all eukaryotes. In unicellular eukaryotes, cell cycle progression is principally governed by one catalytic subunit (cyclin-dependent kinase) that pairs with cell cycle-specific regulatory subunits known as cyclins. Progression through a specific phase of the cell cycle is under the control of a specific class of cyclin. Cell cycle control in multicellular eukaryotes has an additional layer of complexity, as multiple CDKs and cyclins are required. In this review, we will discuss recent advances in the area of cyclins and CDKs, with emphasis on the role of the mammalian proteins in cell cycle control at the cellular and at the organismal level. Many recent surprises have come to light recently as a result of genetic manipulation of cells and mice, and these findings suggest that our understanding of the intricacies of the cell cycle is still rudimentary at best.
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                Author and article information

                Journal
                Onco Targets Ther
                Onco Targets Ther
                OTT
                ott
                OncoTargets and therapy
                Dove
                1178-6930
                10 December 2019
                2019
                : 12
                : 10771-10786
                Affiliations
                [1 ]Central Laboratory, Affiliated Haikou Hospital of Xiangya Medical College, Central South University , Haikou 570208, People’s Republic of China
                [2 ]Clinical Laboratory, The First People’s Hospital of Huaihua , Huaihua 418000, People’s Republic of China
                [3 ]Clinical Laboratory, The First Affiliated Hospital of University of South China , Hengyang 421001, People’s Republic of China
                Author notes
                Correspondence: Shufang Zhang Central Laboratory, Affiliated Haikou Hospital of Xiangya Medical College, Central South University , No.43 Renmin Avenue, Haikou City, Haikou Province570208, People’s Republic of China Email zsf66189665@126.com
                Author information
                http://orcid.org/0000-0003-4894-4951
                http://orcid.org/0000-0002-9927-1622
                Article
                229332
                10.2147/OTT.S229332
                6911351
                06f5fcc2-3def-44f5-9114-acf277f25666
                © 2019 Chen et al.

                This work is published and licensed by Dove Medical Press Limited. The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License ( http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. For permission for commercial use of this work, please see paragraphs 4.2 and 5 of our Terms ( https://www.dovepress.com/terms.php).

                History
                : 30 August 2019
                : 19 November 2019
                Page count
                Figures: 8, Tables: 5, References: 35, Pages: 16
                Funding
                This research was funded by Hainan Provincial Natural Science Foundation of China (Grant No. 2017CXTD010 and 20168312), the National Science Foundation of China (Grant No. 81760465 and 81460450), the Finance science and technology project of hainan province (Grant No. ZDYF2019163 and ZDKJ2017007).
                Categories
                Original Research

                Oncology & Radiotherapy
                bladder cancer,slc35f2,proliferation,migration,invasion
                Oncology & Radiotherapy
                bladder cancer, slc35f2, proliferation, migration, invasion

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