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Print ISSN: 1792-1074 Online ISSN: 1792-1082
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August-2014 Volume 8 Issue 2

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International Journal of Molecular Medicine

International Journal of Molecular Medicine

International Journal of Molecular Medicine is an international journal devoted to molecular mechanisms of human disease.

International Journal of Oncology

International Journal of Oncology

International Journal of Oncology is an international journal devoted to oncology research and cancer treatment.

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Covers molecular medicine topics such as pharmacology, pathology, genetics, neuroscience, infectious diseases, molecular cardiology, and molecular surgery.

Oncology Reports

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Oncology Reports is an international journal devoted to fundamental and applied research in Oncology.

Experimental and Therapeutic Medicine

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Experimental and Therapeutic Medicine is an international journal devoted to laboratory and clinical medicine.

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Oncology Letters

Oncology Letters is an international journal devoted to Experimental and Clinical Oncology.

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Explores a wide range of biological and medical fields, including pharmacology, genetics, microbiology, neuroscience, and molecular cardiology.

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Molecular and Clinical Oncology

International journal addressing all aspects of oncology research, from tumorigenesis and oncogenes to chemotherapy and metastasis.

World Academy of Sciences Journal

World Academy of Sciences Journal

Multidisciplinary open-access journal spanning biochemistry, genetics, neuroscience, environmental health, and synthetic biology.

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International Journal of Functional Nutrition

Open-access journal combining biochemistry, pharmacology, immunology, and genetics to advance health through functional nutrition.

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International Journal of Epigenetics

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Article

Metformin inhibits histone H2B monoubiquitination and downstream gene transcription in human breast cancer cells

  • Authors:
    • Yu Du
    • Haiyan Zheng
    • Jiang Wang
    • Ye Ren
    • Mi Li
    • Chen Gong
    • Fei Xu
    • Caihong Yang
  • View Affiliations / Copyright

    Affiliations: Department of Orthopedics, Tongji Hospital, Huazhong University of Science and Technology, Wuhan, Hubei 430030, P.R. China, Department of Rheumatology, Wuhan Integrated TCM and Western Medicine Hospital (Wuhan No. 1 Hospital), Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei 430030, P.R. China
  • Pages: 809-812
    |
    Published online on: May 19, 2014
       https://doi.org/10.3892/ol.2014.2158
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Abstract

Metformin, one of the most widely prescribed antihyperglycemic drugs, has recently received increasing attention for its potential effects with regard to cancer prevention and treatment. However, the mechanisms behind the suppression of cancer cell growth by metformin remain far from completely understood. The aim of the present study was to investigate whether metformin could regulate histone modification and its downstream gene transcription, and its potential function in inhibiting breast cancer cell proliferation. A T47D cell proliferation curve was determined by cell counting following metformin treatment with differing doses or time courses. The cell cycle was analyzed by flow cytometry with propidium iodide staining. Histone H2B monoubiquitination was evaluated by western blotting subsequent to histone extraction. The histone H2B monoubiquitination downstream gene expression level was determined by quantitative PCR. The results showed that metformin changed the cell‑cycle check‑point and inhibited breast cancer cell proliferation in a dose‑dependent manner. AMPK was activated and histone H2B monoubiquitination and downstream gene transcription were inhibited following metformin treatment in the T47D cells. The effect of metformin on T47D cell proliferation was dependent on AMPK activity. It was concluded that metformin can suppress breast cancer cell growth by the activation of AMPK and the inhibition of histone H2B monoubiquitination and downstream gene transcription. This study reveals a novel potential mechanism of cancer cell growth suppression by metformin.
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Copy and paste a formatted citation
Spandidos Publications style
Du Y, Zheng H, Wang J, Ren Y, Li M, Gong C, Xu F and Yang C: Metformin inhibits histone H2B monoubiquitination and downstream gene transcription in human breast cancer cells. Oncol Lett 8: 809-812, 2014.
APA
Du, Y., Zheng, H., Wang, J., Ren, Y., Li, M., Gong, C. ... Yang, C. (2014). Metformin inhibits histone H2B monoubiquitination and downstream gene transcription in human breast cancer cells. Oncology Letters, 8, 809-812. https://doi.org/10.3892/ol.2014.2158
MLA
Du, Y., Zheng, H., Wang, J., Ren, Y., Li, M., Gong, C., Xu, F., Yang, C."Metformin inhibits histone H2B monoubiquitination and downstream gene transcription in human breast cancer cells". Oncology Letters 8.2 (2014): 809-812.
Chicago
Du, Y., Zheng, H., Wang, J., Ren, Y., Li, M., Gong, C., Xu, F., Yang, C."Metformin inhibits histone H2B monoubiquitination and downstream gene transcription in human breast cancer cells". Oncology Letters 8, no. 2 (2014): 809-812. https://doi.org/10.3892/ol.2014.2158
Copy and paste a formatted citation
x
Spandidos Publications style
Du Y, Zheng H, Wang J, Ren Y, Li M, Gong C, Xu F and Yang C: Metformin inhibits histone H2B monoubiquitination and downstream gene transcription in human breast cancer cells. Oncol Lett 8: 809-812, 2014.
APA
Du, Y., Zheng, H., Wang, J., Ren, Y., Li, M., Gong, C. ... Yang, C. (2014). Metformin inhibits histone H2B monoubiquitination and downstream gene transcription in human breast cancer cells. Oncology Letters, 8, 809-812. https://doi.org/10.3892/ol.2014.2158
MLA
Du, Y., Zheng, H., Wang, J., Ren, Y., Li, M., Gong, C., Xu, F., Yang, C."Metformin inhibits histone H2B monoubiquitination and downstream gene transcription in human breast cancer cells". Oncology Letters 8.2 (2014): 809-812.
Chicago
Du, Y., Zheng, H., Wang, J., Ren, Y., Li, M., Gong, C., Xu, F., Yang, C."Metformin inhibits histone H2B monoubiquitination and downstream gene transcription in human breast cancer cells". Oncology Letters 8, no. 2 (2014): 809-812. https://doi.org/10.3892/ol.2014.2158
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