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International Journal of Oncology
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Print ISSN: 1019-6439 Online ISSN: 1791-2423
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February 2012 Volume 40 Issue 2

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Journals

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.

Molecular Medicine Reports

Molecular Medicine Reports

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

Oncology Reports

Oncology Reports

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

Experimental and Therapeutic Medicine

Experimental and Therapeutic Medicine

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

Oncology Letters

Oncology Letters

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

Biomedical Reports

Biomedical Reports

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

Molecular and Clinical Oncology

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.

International Journal of Functional Nutrition

International Journal of Functional Nutrition

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

International Journal of Epigenetics

International Journal of Epigenetics

Publishes open-access research on using epigenetics to advance understanding and treatment of human disease.

Medicine International

Medicine International

An International Open Access Journal Devoted to General Medicine.

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February 2012 Volume 40 Issue 2

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Article

Activation of AMP-kinase by AICAR induces apoptosis of DU-145 prostate cancer cells through generation of reactive oxygen species and activation of c-Jun N-terminal kinase

  • Authors:
    • Heinrich Sauer
    • Steffi Engel
    • Nada Milosevic
    • Fatemeh Sharifpanah
    • Maria Wartenberg

  • View Affiliations / Copyright

    Affiliations: Department of Physiology, Justus Liebig University Giessen, Aulweg 129, D-35392 Giessen, Germany
  • Pages: 501-508
    |
    Published online on: October 13, 2011
       https://doi.org/10.3892/ijo.2011.1230
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Abstract

The growth of cancer cells is limited by energy supply which is regulated by the energy sensor AMP-kinase (AMPK). Hence, mimicking a low energy state may inhibit cancer growth and may be exploited in anticancer therapies. In the present study, the impact of AMPK activation on cell growth and apoptosis of DU-145 prostate cancer cells was investigated. Incubation with the AMPK activator aminoimidazole carboxamide ribonucleotide (AICAR) dose-dependently inhibited cell growth, activated AMPK, and inhibited mTOR. Furthermore, AICAR treatment activated c-Jun N-terminal kinase (JNK) and caspase-3, thereby initiating apoptosis. Within 60 min of treatment AICAR raised intracellular reactive oxygen species (ROS) which could be abolished in the presence of the free radical scavenger N-(2-mercaptopropionyl)glycin (NMPG), the AMPK inhibitor compound C (Comp C) and the respiratory chain complex I inhibitor rotenone, but not by the NADPH oxidase inhibitor VAS2870. Inhibition of ROS generation abolished AMPK activation by AICAR as well as JNK and caspase-3 activation. Furthermore, AMPK activation, JNK phosphorylation and cleaved caspase-3 upon AICAR treatment were abolished in the presence of Comp C. In summary, our data demonstrate that activation of AMPK by AICAR induces apoptosis of prostate cancer cells by a signaling pathway involving ROS, activation of JNK and cleaved caspase-3.

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Copy and paste a formatted citation
Spandidos Publications style
Sauer H, Engel S, Milosevic N, Sharifpanah F and Wartenberg M: Activation of AMP-kinase by AICAR induces apoptosis of DU-145 prostate cancer cells through generation of reactive oxygen species and activation of c-Jun N-terminal kinase. Int J Oncol 40: 501-508, 2012.
APA
Sauer, H., Engel, S., Milosevic, N., Sharifpanah, F., & Wartenberg, M. (2012). Activation of AMP-kinase by AICAR induces apoptosis of DU-145 prostate cancer cells through generation of reactive oxygen species and activation of c-Jun N-terminal kinase. International Journal of Oncology, 40, 501-508. https://doi.org/10.3892/ijo.2011.1230
MLA
Sauer, H., Engel, S., Milosevic, N., Sharifpanah, F., Wartenberg, M."Activation of AMP-kinase by AICAR induces apoptosis of DU-145 prostate cancer cells through generation of reactive oxygen species and activation of c-Jun N-terminal kinase". International Journal of Oncology 40.2 (2012): 501-508.
Chicago
Sauer, H., Engel, S., Milosevic, N., Sharifpanah, F., Wartenberg, M."Activation of AMP-kinase by AICAR induces apoptosis of DU-145 prostate cancer cells through generation of reactive oxygen species and activation of c-Jun N-terminal kinase". International Journal of Oncology 40, no. 2 (2012): 501-508. https://doi.org/10.3892/ijo.2011.1230
Copy and paste a formatted citation
x
Spandidos Publications style
Sauer H, Engel S, Milosevic N, Sharifpanah F and Wartenberg M: Activation of AMP-kinase by AICAR induces apoptosis of DU-145 prostate cancer cells through generation of reactive oxygen species and activation of c-Jun N-terminal kinase. Int J Oncol 40: 501-508, 2012.
APA
Sauer, H., Engel, S., Milosevic, N., Sharifpanah, F., & Wartenberg, M. (2012). Activation of AMP-kinase by AICAR induces apoptosis of DU-145 prostate cancer cells through generation of reactive oxygen species and activation of c-Jun N-terminal kinase. International Journal of Oncology, 40, 501-508. https://doi.org/10.3892/ijo.2011.1230
MLA
Sauer, H., Engel, S., Milosevic, N., Sharifpanah, F., Wartenberg, M."Activation of AMP-kinase by AICAR induces apoptosis of DU-145 prostate cancer cells through generation of reactive oxygen species and activation of c-Jun N-terminal kinase". International Journal of Oncology 40.2 (2012): 501-508.
Chicago
Sauer, H., Engel, S., Milosevic, N., Sharifpanah, F., Wartenberg, M."Activation of AMP-kinase by AICAR induces apoptosis of DU-145 prostate cancer cells through generation of reactive oxygen species and activation of c-Jun N-terminal kinase". International Journal of Oncology 40, no. 2 (2012): 501-508. https://doi.org/10.3892/ijo.2011.1230
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