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Wnt Signaling Inhibits the Growth of Primary Cilia and Activates CyclinD1, Snail and VEGFA Expression in Breast Cancer Cell Line MDA-MB-231

Received: 23 March 2015     Accepted: 31 March 2015     Published: 21 April 2015
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Abstract

Although Wnt/β-catenin signaling has been shown to be essential in the process of cancer formation, it is unclear how Wnt3a signaling pathway regulates abnormal proliferation and differentiation of breast cancer cells. Here, we found overexpression of Wnt3a stimulated the expression of the Wntsignaling’s downstream genes such as LRP6, Naked, Axin1, DVL-2, β-catenin, and TCF-1 in breast cancer cell line MDA-MB-231.Primarycilia is deemed as sensory cell antennae thatcoordinates a large number of cellular signaling pathways, sometimes coupling cell division and differentiation. Primary cilia were found on the surface of this cell line. Overexpression of Wnt3a decreased the formation of primary cilia. Inhibition of Wnt3a with Calphostin C facilitated growth of primary cilia. Wnt3a activated cell proliferation gene of CyclinD1. In contrary, Calphostin C decreased the promotional effect on proliferation of MDA-MB-231. The Snail family of transcription factor has previously been implicated in the differentiation of epithelial cells into mesenchymal cells (epithelial-mesenchymal transitions) during embryonic development. Wnt3a promoted MDA-MB-231 induced expression of Snail, whose effect was inhibited by Calphostin-C. VEGFA activity was originally referred to as vascular permeability factor and had been shown to stimulate endothelial cell mitogenesis and cell migration and increased microvascular permeability. Wnt3a facilitated MDA-MB-231 induced expression of VEGFA, as well as Calphostin-C suppressed its effect. Taken together, these results suggested thatWnt3a signaling played an important role in regulating the formation of breast cancer.

Published in American Journal of Life Sciences (Volume 3, Issue 3)
DOI 10.11648/j.ajls.20150303.11
Page(s) 123-133
Creative Commons

This is an Open Access article, distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution and reproduction in any medium or format, provided the original work is properly cited.

Copyright

Copyright © The Author(s), 2015. Published by Science Publishing Group

Keywords

Wnt3a, Wnt Signaling, Breast Cancer, Calphostin C, Primary Cilia

References
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  • APA Style

    Xiaoyan Deng, Ning Hu, Lifu Wang, Feilong Li, Geli Liu, et al. (2015). Wnt Signaling Inhibits the Growth of Primary Cilia and Activates CyclinD1, Snail and VEGFA Expression in Breast Cancer Cell Line MDA-MB-231. American Journal of Life Sciences, 3(3), 123-133. https://doi.org/10.11648/j.ajls.20150303.11

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    ACS Style

    Xiaoyan Deng; Ning Hu; Lifu Wang; Feilong Li; Geli Liu, et al. Wnt Signaling Inhibits the Growth of Primary Cilia and Activates CyclinD1, Snail and VEGFA Expression in Breast Cancer Cell Line MDA-MB-231. Am. J. Life Sci. 2015, 3(3), 123-133. doi: 10.11648/j.ajls.20150303.11

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    AMA Style

    Xiaoyan Deng, Ning Hu, Lifu Wang, Feilong Li, Geli Liu, et al. Wnt Signaling Inhibits the Growth of Primary Cilia and Activates CyclinD1, Snail and VEGFA Expression in Breast Cancer Cell Line MDA-MB-231. Am J Life Sci. 2015;3(3):123-133. doi: 10.11648/j.ajls.20150303.11

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  • @article{10.11648/j.ajls.20150303.11,
      author = {Xiaoyan Deng and Ning Hu and Lifu Wang and Feilong Li and Geli Liu and Xiangmei Wu and Chengfu Yuan and Zunpeng Liu and Jiachuan Pan and Changdong Wang},
      title = {Wnt Signaling Inhibits the Growth of Primary Cilia and Activates CyclinD1, Snail and VEGFA Expression in Breast Cancer Cell Line MDA-MB-231},
      journal = {American Journal of Life Sciences},
      volume = {3},
      number = {3},
      pages = {123-133},
      doi = {10.11648/j.ajls.20150303.11},
      url = {https://doi.org/10.11648/j.ajls.20150303.11},
      eprint = {https://article.sciencepublishinggroup.com/pdf/10.11648.j.ajls.20150303.11},
      abstract = {Although Wnt/β-catenin signaling has been shown to be essential in the process of cancer formation, it is unclear how Wnt3a signaling pathway regulates abnormal proliferation and differentiation of breast cancer cells. Here, we found overexpression of Wnt3a stimulated the expression of the Wntsignaling’s downstream genes such as LRP6, Naked, Axin1, DVL-2, β-catenin, and TCF-1 in breast cancer cell line MDA-MB-231.Primarycilia is deemed as sensory cell antennae thatcoordinates a large number of cellular signaling pathways, sometimes coupling cell division and differentiation. Primary cilia were found on the surface of this cell line. Overexpression of Wnt3a decreased the formation of primary cilia. Inhibition of Wnt3a with Calphostin C facilitated growth of primary cilia. Wnt3a activated cell proliferation gene of CyclinD1. In contrary, Calphostin C decreased the promotional effect on proliferation of MDA-MB-231. The Snail family of transcription factor has previously been implicated in the differentiation of epithelial cells into mesenchymal cells (epithelial-mesenchymal transitions) during embryonic development. Wnt3a promoted MDA-MB-231 induced expression of Snail, whose effect was inhibited by Calphostin-C. VEGFA activity was originally referred to as vascular permeability factor and had been shown to stimulate endothelial cell mitogenesis and cell migration and increased microvascular permeability. Wnt3a facilitated MDA-MB-231 induced expression of VEGFA, as well as Calphostin-C suppressed its effect. Taken together, these results suggested thatWnt3a signaling played an important role in regulating the formation of breast cancer.},
     year = {2015}
    }
    

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  • TY  - JOUR
    T1  - Wnt Signaling Inhibits the Growth of Primary Cilia and Activates CyclinD1, Snail and VEGFA Expression in Breast Cancer Cell Line MDA-MB-231
    AU  - Xiaoyan Deng
    AU  - Ning Hu
    AU  - Lifu Wang
    AU  - Feilong Li
    AU  - Geli Liu
    AU  - Xiangmei Wu
    AU  - Chengfu Yuan
    AU  - Zunpeng Liu
    AU  - Jiachuan Pan
    AU  - Changdong Wang
    Y1  - 2015/04/21
    PY  - 2015
    N1  - https://doi.org/10.11648/j.ajls.20150303.11
    DO  - 10.11648/j.ajls.20150303.11
    T2  - American Journal of Life Sciences
    JF  - American Journal of Life Sciences
    JO  - American Journal of Life Sciences
    SP  - 123
    EP  - 133
    PB  - Science Publishing Group
    SN  - 2328-5737
    UR  - https://doi.org/10.11648/j.ajls.20150303.11
    AB  - Although Wnt/β-catenin signaling has been shown to be essential in the process of cancer formation, it is unclear how Wnt3a signaling pathway regulates abnormal proliferation and differentiation of breast cancer cells. Here, we found overexpression of Wnt3a stimulated the expression of the Wntsignaling’s downstream genes such as LRP6, Naked, Axin1, DVL-2, β-catenin, and TCF-1 in breast cancer cell line MDA-MB-231.Primarycilia is deemed as sensory cell antennae thatcoordinates a large number of cellular signaling pathways, sometimes coupling cell division and differentiation. Primary cilia were found on the surface of this cell line. Overexpression of Wnt3a decreased the formation of primary cilia. Inhibition of Wnt3a with Calphostin C facilitated growth of primary cilia. Wnt3a activated cell proliferation gene of CyclinD1. In contrary, Calphostin C decreased the promotional effect on proliferation of MDA-MB-231. The Snail family of transcription factor has previously been implicated in the differentiation of epithelial cells into mesenchymal cells (epithelial-mesenchymal transitions) during embryonic development. Wnt3a promoted MDA-MB-231 induced expression of Snail, whose effect was inhibited by Calphostin-C. VEGFA activity was originally referred to as vascular permeability factor and had been shown to stimulate endothelial cell mitogenesis and cell migration and increased microvascular permeability. Wnt3a facilitated MDA-MB-231 induced expression of VEGFA, as well as Calphostin-C suppressed its effect. Taken together, these results suggested thatWnt3a signaling played an important role in regulating the formation of breast cancer.
    VL  - 3
    IS  - 3
    ER  - 

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Author Information
  • Department of Biochemistry and Molecular Biology, Functional Genomics Lab, Molecular Medicine and Cancer Research Center, Chongqing Medical University, Chongqing, China

  • Department of Orthopaedic Surgery, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China

  • Department of Biochemistry and Molecular Biology, Functional Genomics Lab, Molecular Medicine and Cancer Research Center, Chongqing Medical University, Chongqing, China

  • Department of Biochemistry and Molecular Biology, Functional Genomics Lab, Molecular Medicine and Cancer Research Center, Chongqing Medical University, Chongqing, China

  • Department of Biochemistry and Molecular Biology, Functional Genomics Lab, Molecular Medicine and Cancer Research Center, Chongqing Medical University, Chongqing, China

  • Department of Biochemistry and Molecular Biology, Functional Genomics Lab, Molecular Medicine and Cancer Research Center, Chongqing Medical University, Chongqing, China

  • Department of Biochemistry & Molecular Biology, College of Medical Science, China Three Gorges University, Yichang, HuBei, China

  • Department of Orthopaedics, The Fourth Affiliated Hospital of China Medical University, Shenyang, China

  • Department of Biomedical and Chemical Engineering, Syracuse University, Syracuse, New York, United States of America

  • Department of Biochemistry and Molecular Biology, Functional Genomics Lab, Molecular Medicine and Cancer Research Center, Chongqing Medical University, Chongqing, China

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