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Oncology Reports
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Print ISSN: 1021-335X Online ISSN: 1791-2431
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March 2009 Volume 21 Issue 3

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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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Article

Gefitinib circumvents hypoxia-induced drug resistance by the modulation of HIF-1α

  • Authors:
    • Jin Kyung Rho
    • Yun Jung Choi
    • Jin Kyung Lee
    • Baek-Yeol Ryoo
    • Im Ii Na
    • Sung Hyun Yang
    • Cheol Hyeon Kim
    • Young Do Yoo
    • Jae Cheol Lee

  • View Affiliations / Copyright

    Affiliations: Department of Internal Medicine, Korea Cancer Center Hospital, Korea Institute of Radiological and Medical Science, Seoul 139-706, Korea
  • Pages: 801-807
    |
    Published online on: March 1, 2009
       https://doi.org/10.3892/or_00000287
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Abstract

Hypoxia-inducible factor-1α (HIF-1α) is a transcriptional factor which is activated by hypoxia and associated with cell survival, proliferation and drug resistance. Recent studies have shown that the down-stream molecules of the epidermal growth factor receptor (EGFR) signal are involved in the hypoxia-dependent or -independent HIF-1α protein accumulation. Thus, we hypothesized that an EGFR-TK inhibitor, gefitinib, might circumvent the hypoxia-induced drug resistance via the regulation of HIF-1α expression. In our data, treatment of gefitinib suppressed induced HIF-1α by hypoxia. This action of gefitinib was caused by reduced protein stability without any change in the level of HIF-1α mRNA. The effect of gefitinib on down-regulation of HIF-1α was reversed by transfection of constitutively active form of Akt. The cellular response to gefitinib was similar in both normoxia and hypoxia condition. However, the response to conventional chemotherapeutic drugs decreased >50% under hypoxia condition and they did not change HIF-1α expression. In addition, the suppression of HIF-1α using siRNA overcame partially hypoxia-induced drug resistance. In conclusion, gefitinib was able to circumvent hypoxia-induced drug resistance suggesting that the effective suppression of HIF-1α by the inhibition of EGFR-Akt pathway may overcome the hypoxia-induced drug resistance.

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Copy and paste a formatted citation
Spandidos Publications style
Rho JK, Choi YJ, Lee JK, Ryoo B, Na II, Yang SH, Kim CH, Yoo YD and Lee JC: Gefitinib circumvents hypoxia-induced drug resistance by the modulation of HIF-1α. Oncol Rep 21: 801-807, 2009.
APA
Rho, J.K., Choi, Y.J., Lee, J.K., Ryoo, B., Na, I.I., Yang, S.H. ... Lee, J.C. (2009). Gefitinib circumvents hypoxia-induced drug resistance by the modulation of HIF-1α. Oncology Reports, 21, 801-807. https://doi.org/10.3892/or_00000287
MLA
Rho, J. K., Choi, Y. J., Lee, J. K., Ryoo, B., Na, I. I., Yang, S. H., Kim, C. H., Yoo, Y. D., Lee, J. C."Gefitinib circumvents hypoxia-induced drug resistance by the modulation of HIF-1α". Oncology Reports 21.3 (2009): 801-807.
Chicago
Rho, J. K., Choi, Y. J., Lee, J. K., Ryoo, B., Na, I. I., Yang, S. H., Kim, C. H., Yoo, Y. D., Lee, J. C."Gefitinib circumvents hypoxia-induced drug resistance by the modulation of HIF-1α". Oncology Reports 21, no. 3 (2009): 801-807. https://doi.org/10.3892/or_00000287
Copy and paste a formatted citation
x
Spandidos Publications style
Rho JK, Choi YJ, Lee JK, Ryoo B, Na II, Yang SH, Kim CH, Yoo YD and Lee JC: Gefitinib circumvents hypoxia-induced drug resistance by the modulation of HIF-1α. Oncol Rep 21: 801-807, 2009.
APA
Rho, J.K., Choi, Y.J., Lee, J.K., Ryoo, B., Na, I.I., Yang, S.H. ... Lee, J.C. (2009). Gefitinib circumvents hypoxia-induced drug resistance by the modulation of HIF-1α. Oncology Reports, 21, 801-807. https://doi.org/10.3892/or_00000287
MLA
Rho, J. K., Choi, Y. J., Lee, J. K., Ryoo, B., Na, I. I., Yang, S. H., Kim, C. H., Yoo, Y. D., Lee, J. C."Gefitinib circumvents hypoxia-induced drug resistance by the modulation of HIF-1α". Oncology Reports 21.3 (2009): 801-807.
Chicago
Rho, J. K., Choi, Y. J., Lee, J. K., Ryoo, B., Na, I. I., Yang, S. H., Kim, C. H., Yoo, Y. D., Lee, J. C."Gefitinib circumvents hypoxia-induced drug resistance by the modulation of HIF-1α". Oncology Reports 21, no. 3 (2009): 801-807. https://doi.org/10.3892/or_00000287
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