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International Journal of Oncology
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Print ISSN: 1019-6439 Online ISSN: 1791-2423
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January 2011 Volume 38 Issue 1

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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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January 2011 Volume 38 Issue 1

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Article

TRAIL-induced caspase/p38 activation is responsible for the increased catalytic and invasive activities of Akt

  • Authors:
    • Bo K. Sun
    • Joo-Hang Kim
    • Hoan N. Nguyen
    • So Y. Kim
    • Seeun Oh
    • Yong J. Lee
    • Jae J. Song

  • View Affiliations / Copyright

    Affiliations: Institute for Cancer Research, Yonsei Cancer Center, Yonsei University, Seoul 120-752, Republic of Korea
  • Pages: 249-256
    |
    Published online on: January 1, 2011
       https://doi.org/10.3892/ijo_00000845
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Abstract

We previously observed that TRAIL induces acquired TRAIL resistance coinciding with increased Akt phosphorylation brought about by the Src-PI3K-Akt signaling pathways and mediated by c-Cbl. c-Cbl, a ubiquitously expressed cytoplasmic adaptor protein, is simultaneously involved in the rapid degradation of TRAIL receptors and Akt phosphorylation during TRAIL treatment. Here, we show that Akt phosphorylation is not exclusively responsible for acquired TRAIL resistance. Akt catalytic activation is known to increase during metabolic oxidative stress, but we show that TRAIL also dramatically induces the catalytic activation of Akt in TRAIL-sensitive cells, but not in TRAIL-resistant cells. This suggests that Akt catalytic activation during TRAIL-induced apoptosis is likely to play a compensatory role in the maintenance of cell homeostasis. In addition, activated p38 and phosphorylated HSP27 were found to act as downstream effector molecules of p38 during TRAIL treatment and were shown to be responsible for increased Akt catalytic and invasive activities.

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Copy and paste a formatted citation
Spandidos Publications style
Sun BK, Kim J, Nguyen HN, Kim SY, Oh S, Lee YJ and Song JJ: TRAIL-induced caspase/p38 activation is responsible for the increased catalytic and invasive activities of Akt. Int J Oncol 38: 249-256, 2011.
APA
Sun, B.K., Kim, J., Nguyen, H.N., Kim, S.Y., Oh, S., Lee, Y.J., & Song, J.J. (2011). TRAIL-induced caspase/p38 activation is responsible for the increased catalytic and invasive activities of Akt. International Journal of Oncology, 38, 249-256. https://doi.org/10.3892/ijo_00000845
MLA
Sun, B. K., Kim, J., Nguyen, H. N., Kim, S. Y., Oh, S., Lee, Y. J., Song, J. J."TRAIL-induced caspase/p38 activation is responsible for the increased catalytic and invasive activities of Akt". International Journal of Oncology 38.1 (2011): 249-256.
Chicago
Sun, B. K., Kim, J., Nguyen, H. N., Kim, S. Y., Oh, S., Lee, Y. J., Song, J. J."TRAIL-induced caspase/p38 activation is responsible for the increased catalytic and invasive activities of Akt". International Journal of Oncology 38, no. 1 (2011): 249-256. https://doi.org/10.3892/ijo_00000845
Copy and paste a formatted citation
x
Spandidos Publications style
Sun BK, Kim J, Nguyen HN, Kim SY, Oh S, Lee YJ and Song JJ: TRAIL-induced caspase/p38 activation is responsible for the increased catalytic and invasive activities of Akt. Int J Oncol 38: 249-256, 2011.
APA
Sun, B.K., Kim, J., Nguyen, H.N., Kim, S.Y., Oh, S., Lee, Y.J., & Song, J.J. (2011). TRAIL-induced caspase/p38 activation is responsible for the increased catalytic and invasive activities of Akt. International Journal of Oncology, 38, 249-256. https://doi.org/10.3892/ijo_00000845
MLA
Sun, B. K., Kim, J., Nguyen, H. N., Kim, S. Y., Oh, S., Lee, Y. J., Song, J. J."TRAIL-induced caspase/p38 activation is responsible for the increased catalytic and invasive activities of Akt". International Journal of Oncology 38.1 (2011): 249-256.
Chicago
Sun, B. K., Kim, J., Nguyen, H. N., Kim, S. Y., Oh, S., Lee, Y. J., Song, J. J."TRAIL-induced caspase/p38 activation is responsible for the increased catalytic and invasive activities of Akt". International Journal of Oncology 38, no. 1 (2011): 249-256. https://doi.org/10.3892/ijo_00000845
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