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Progesterone Induces NFκB DNA Binding Activity through a PI3K/Akt-Dependent Pathway in MCF-7 Breast Cancer Cells

Received: 13 June 2014     Accepted: 28 June 2014     Published: 10 July 2014
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Abstract

Progesterone (PG) is a steroid hormone that regulates normal reproductive functions including uterine and mammary gland development. The PG receptor belongs to the nuclear receptor superfamily of ligand dependent transcription factors that mediates gene expression, however, it also promotes cell signaling pathways through a non-genomic pathway including the activation of PI3K/Akt and Src/ERK1/2 pathways. However the role of PG in NFκB-DNA complex formation remains to be studied. We demonstrate here that PG induces Akt2 activation and an increase of NFκB DNA binding activity in MCF-7 breast cancer cells. Akt2 activation requires PI3K activity, whereas increase of NFκB DNA binding activity requires PI3K, mTOR, Akt, Src, and G-proteins activity, as well as the integrity of cytoskeleton. In summary, our findings demonstrate that PG induces an increase of NFκB DNA binding activity in MCF-7 cells.

Published in Cancer Research Journal (Volume 2, Issue 4)
DOI 10.11648/j.crj.20140204.11
Page(s) 63-69
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), 2014. Published by Science Publishing Group

Keywords

Breast Cancer, Progesterone, PI3K/Akt, NFκB, MCF-7

References
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Cite This Article
  • APA Style

    Fernando Candanedo-Gonzalez, Octavio Galindo-Hernandez, Nathalia Serna-Marquez, Roberto Espinosa-Neira, Adriana Soto-Guzman, et al. (2014). Progesterone Induces NFκB DNA Binding Activity through a PI3K/Akt-Dependent Pathway in MCF-7 Breast Cancer Cells. Cancer Research Journal, 2(4), 63-69. https://doi.org/10.11648/j.crj.20140204.11

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    ACS Style

    Fernando Candanedo-Gonzalez; Octavio Galindo-Hernandez; Nathalia Serna-Marquez; Roberto Espinosa-Neira; Adriana Soto-Guzman, et al. Progesterone Induces NFκB DNA Binding Activity through a PI3K/Akt-Dependent Pathway in MCF-7 Breast Cancer Cells. Cancer Res. J. 2014, 2(4), 63-69. doi: 10.11648/j.crj.20140204.11

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    AMA Style

    Fernando Candanedo-Gonzalez, Octavio Galindo-Hernandez, Nathalia Serna-Marquez, Roberto Espinosa-Neira, Adriana Soto-Guzman, et al. Progesterone Induces NFκB DNA Binding Activity through a PI3K/Akt-Dependent Pathway in MCF-7 Breast Cancer Cells. Cancer Res J. 2014;2(4):63-69. doi: 10.11648/j.crj.20140204.11

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  • @article{10.11648/j.crj.20140204.11,
      author = {Fernando Candanedo-Gonzalez and Octavio Galindo-Hernandez and Nathalia Serna-Marquez and Roberto Espinosa-Neira and Adriana Soto-Guzman and Pedro Cortes-Reynosa and Eduardo Perez Salazar},
      title = {Progesterone Induces NFκB DNA Binding Activity through a PI3K/Akt-Dependent Pathway in MCF-7 Breast Cancer Cells},
      journal = {Cancer Research Journal},
      volume = {2},
      number = {4},
      pages = {63-69},
      doi = {10.11648/j.crj.20140204.11},
      url = {https://doi.org/10.11648/j.crj.20140204.11},
      eprint = {https://article.sciencepublishinggroup.com/pdf/10.11648.j.crj.20140204.11},
      abstract = {Progesterone (PG) is a steroid hormone that regulates normal reproductive functions including uterine and mammary gland development. The PG receptor belongs to the nuclear receptor superfamily of ligand dependent transcription factors that mediates gene expression, however, it also promotes cell signaling pathways through a non-genomic pathway including the activation of PI3K/Akt and Src/ERK1/2 pathways. However the role of PG in NFκB-DNA complex formation remains to be studied. We demonstrate here that PG induces Akt2 activation and an increase of NFκB DNA binding activity in MCF-7 breast cancer cells. Akt2 activation requires PI3K activity, whereas increase of NFκB DNA binding activity requires PI3K, mTOR, Akt, Src, and G-proteins activity, as well as the integrity of cytoskeleton. In summary, our findings demonstrate that PG induces an increase of NFκB DNA binding activity in MCF-7 cells.},
     year = {2014}
    }
    

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  • TY  - JOUR
    T1  - Progesterone Induces NFκB DNA Binding Activity through a PI3K/Akt-Dependent Pathway in MCF-7 Breast Cancer Cells
    AU  - Fernando Candanedo-Gonzalez
    AU  - Octavio Galindo-Hernandez
    AU  - Nathalia Serna-Marquez
    AU  - Roberto Espinosa-Neira
    AU  - Adriana Soto-Guzman
    AU  - Pedro Cortes-Reynosa
    AU  - Eduardo Perez Salazar
    Y1  - 2014/07/10
    PY  - 2014
    N1  - https://doi.org/10.11648/j.crj.20140204.11
    DO  - 10.11648/j.crj.20140204.11
    T2  - Cancer Research Journal
    JF  - Cancer Research Journal
    JO  - Cancer Research Journal
    SP  - 63
    EP  - 69
    PB  - Science Publishing Group
    SN  - 2330-8214
    UR  - https://doi.org/10.11648/j.crj.20140204.11
    AB  - Progesterone (PG) is a steroid hormone that regulates normal reproductive functions including uterine and mammary gland development. The PG receptor belongs to the nuclear receptor superfamily of ligand dependent transcription factors that mediates gene expression, however, it also promotes cell signaling pathways through a non-genomic pathway including the activation of PI3K/Akt and Src/ERK1/2 pathways. However the role of PG in NFκB-DNA complex formation remains to be studied. We demonstrate here that PG induces Akt2 activation and an increase of NFκB DNA binding activity in MCF-7 breast cancer cells. Akt2 activation requires PI3K activity, whereas increase of NFκB DNA binding activity requires PI3K, mTOR, Akt, Src, and G-proteins activity, as well as the integrity of cytoskeleton. In summary, our findings demonstrate that PG induces an increase of NFκB DNA binding activity in MCF-7 cells.
    VL  - 2
    IS  - 4
    ER  - 

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Author Information
  • Departamento de Biologia Celular. Cinvestav-IPN. Av IPN # 2508. San Pedro Zacatenco. Mexico, DF. 07360. Mexico

  • Departamento de Biologia Celular. Cinvestav-IPN. Av IPN # 2508. San Pedro Zacatenco. Mexico, DF. 07360. Mexico

  • Departamento de Biologia Celular. Cinvestav-IPN. Av IPN # 2508. San Pedro Zacatenco. Mexico, DF. 07360. Mexico

  • Departamento de Biologia Celular. Cinvestav-IPN. Av IPN # 2508. San Pedro Zacatenco. Mexico, DF. 07360. Mexico

  • Departamento de Biologia Celular. Cinvestav-IPN. Av IPN # 2508. San Pedro Zacatenco. Mexico, DF. 07360. Mexico

  • Departamento de Biologia Celular. Cinvestav-IPN. Av IPN # 2508. San Pedro Zacatenco. Mexico, DF. 07360. Mexico

  • Departamento de Biologia Celular. Cinvestav-IPN. Av IPN # 2508. San Pedro Zacatenco. Mexico, DF. 07360. Mexico

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