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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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      Is Open Access

      Knockdown of KIF26B inhibits breast cancer cell proliferation, migration, and invasion

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          Abstract

          Background

          Kinesin family member 26B (KIF26B) plays a key role in the development and progression of many human cancers. However, the role and underlying mechanisms of KIF26B in breast cancer cells remain unknown.

          Materials and methods

          In this study, we inhibited the expression of KIF26B in MDA-MB-231 and MCF-7 cells using lentivirus-delivered shRNA.

          Results

          Lentivirus-mediated KIF26B knockdown significantly suppressed cell proliferation, colony formation, migration, and invasion. Furthermore, cell cycle analyses revealed that the percentage of cells in the G0/G1 phase was significantly increased in KIF26B knockdown cells. Moreover, the knockdown of KIF26B significantly promoted cell apoptosis via the upregulation of cleaved caspase-3 and Bax.

          Conclusion

          Our data indicate that KIF26B plays a pivotal role in tumor growth and metastasis in breast cancer cells and may be a potential therapeutic target for treating breast cancer.

          Most cited references17

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          Breast cancer metastasis: markers and models.

          Britta Weigelt, Johannes Peterse, Laura J van 't Veer (2005)
          Breast cancer starts as a local disease, but it can metastasize to the lymph nodes and distant organs. At primary diagnosis, prognostic markers are used to assess whether the transition to systemic disease is likely to have occurred. The prevailing model of metastasis reflects this view--it suggests that metastatic capacity is a late, acquired event in tumorigenesis. Others have proposed the idea that breast cancer is intrinsically a systemic disease. New molecular technologies, such as DNA microarrays, support the idea that metastatic capacity might be an inherent feature of breast tumours. These data have important implications for prognosis prediction and our understanding of metastasis.
          Article 0 comments Cited 728 times – based on 0 reviews     Review now
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            Kinesin superfamily motor proteins and intracellular transport.

            Nobutaka Hirokawa, Yasuko Noda, Yosuke Tanaka … (2009)
            Intracellular transport is fundamental for cellular function, survival and morphogenesis. Kinesin superfamily proteins (also known as KIFs) are important molecular motors that directionally transport various cargos, including membranous organelles, protein complexes and mRNAs. The mechanisms by which different kinesins recognize and bind to specific cargos, as well as how kinesins unload cargo and determine the direction of transport, have now been identified. Furthermore, recent molecular genetic experiments have uncovered important and unexpected roles for kinesins in the regulation of such physiological processes as higher brain function, tumour suppression and developmental patterning. These findings open exciting new areas of kinesin research.
            Article 0 comments Cited 561 times – based on 0 reviews     Review now
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              Multiple levels of cyclin specificity in cell-cycle control.

              Joanna Bloom, Frederick R. Cross (2007)
              Cyclins regulate the cell cycle by binding to and activating cyclin-dependent kinases (Cdks). Phosphorylation of specific targets by cyclin-Cdk complexes sets in motion different processes that drive the cell cycle in a timely manner. In budding yeast, a single Cdk is activated by multiple cyclins. The ability of these cyclins to target specific proteins and to initiate different cell-cycle events might, in some cases, reflect the timing of the expression of the cyclins; in others, it might reflect intrinsic properties of the cyclins that render them better suited to target particular proteins.
              Article 0 comments Cited 151 times – based on 0 reviews     Review now
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                Author and article information

                Journal
                Journal ID (nlm-ta): Onco Targets Ther
                Journal ID (iso-abbrev): Onco Targets Ther
                Journal ID (publisher-id): OncoTargets and Therapy
                Title: OncoTargets and therapy
                Publisher: Dove Medical Press
                ISSN (Electronic): 1178-6930
                Publication date Collection: 2018
                Publication date (Electronic): 29 May 2018
                Volume: 11
                Pages: 3195-3203
                Affiliations
                [1 ]Department of Oncology, Affiliated Hospital of Nantong University, Nantong 226001, China
                [2 ]Department of General Surgery, Xinhua Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200092, China
                [3 ]Medical College of Nantong University, Nantong 226001, China
                [4 ]Department of Endoscopic Diagnosis and Treatment of Digestive Diseases, Xinhua Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200092, China
                [5 ]Department of Pathology, Affiliated Hospital of Nantong University, Nantong 226001, China
                Author notes
                Correspondence: Li Qian, Department of Oncology, Affiliated Hospital of Nantong University, 20 Xisi Road, Nantong 226001, Jiangsu Province, China, Email qianlint@ 123456foxmail.com
                Shu Zhang, Department of Pathology, Affiliated Hospital of Nantong University, 20 Xisi Road, Nantong 226001, Jiangsu Province, China, Email YLTD66@ 123456126.com
                [*]

                These authors contributed equally to this work

                Article
                Publisher ID: ott-11-3195
                DOI: 10.2147/OTT.S163346
                PMC ID: 5985780
                PubMed ID: 29881293
                SO-VID: 906108c2-c594-41a6-9cbc-9cde2f4fd027
                Copyright © © 2018 Gu et al. This work is published and licensed by Dove Medical Press Limited
                License:

                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.

                History
                Categories
                Subject: Original Research

                ScienceOpen disciplines: Oncology & Radiotherapy
                Keywords: kif26b,breast cancer cell,proliferation,migration,invasion
                Data availability:
                ScienceOpen disciplines: Oncology & Radiotherapy
                Keywords: kif26b, breast cancer cell, proliferation, migration, invasion

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