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International Journal of Oncology
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Print ISSN: 1019-6439 Online ISSN: 1791-2423
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August 2012 Volume 41 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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Molecular Medicine Reports

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 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.

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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

uPAR and cathepsin B knockdown inhibits radiation-induced PKC integrated integrin signaling to the cytoskeleton of glioma-initiating cells

  • Authors:
    • Kiranmai Alapati
    • Sreelatha Gopinath
    • Rama Rao Malla
    • Venkata Ramesh Dasari
    • Jasti S. Rao
  • View Affiliations / Copyright

    Affiliations: Department of Cancer Biology and Pharmacology, University of Illinois College of Medicine at Peoria, Peoria, IL 61605, USA
  • Pages: 599-610
    |
    Published online on: May 24, 2012
       https://doi.org/10.3892/ijo.2012.1496
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Abstract

Despite advances in radiotherapeutic and chemotherapeutic techniques and aggressive surgical resection, the prognosis of glioblastoma patients is dismal. Accumulation of evidence indicates that some cancer cells survive even the most aggressive treatments, and these surviving cells, which are resistant to therapy and are perhaps essential for the malignancy, may be cancer stem cells. The CD133 surface marker is commonly used to isolate these extremely resistant glioma-initiating cells (GICs). In the present study, GICs which tested positive for the CD133 marker (CD133+) were isolated from both the established U251 cell line and the 5310 xenograft glioma cell line to study the events related to the molecular pathogenesis of these cells. Simultaneous down-regulation of uPAR and cathepsin B by shRNA (pUC) treatment caused the disruption of radiation-induced complex formation of pPKC θ/δ, integrin β1 and PKC ζ, integrin β1 in glioma cells. Further, pUC treatment inhibited PKC/integrin signaling via FAK by causing disassociation of FAK and the cytoskeletal molecules vinculin and α-actinin. Also, we observed the inhibition of ERK phosphorylation. This inhibition was mediated by pUC and directed a negative feedback mechanism over the FAK signaling molecules, which led to an extensive reduction in the signal for cytoskeletal organization generating migratory arrest. Altogether, it can be hypothesized that knockdown of uPAR and cathepsin B using shRNA is an effective strategy for controlling highly invasive glioma cells and extremely resistant glioma-initiating cells.
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Copy and paste a formatted citation
Spandidos Publications style
Alapati K, Gopinath S, Malla RR, Dasari VR and Rao JS: uPAR and cathepsin B knockdown inhibits radiation-induced PKC integrated integrin signaling to the cytoskeleton of glioma-initiating cells. Int J Oncol 41: 599-610, 2012.
APA
Alapati, K., Gopinath, S., Malla, R.R., Dasari, V.R., & Rao, J.S. (2012). uPAR and cathepsin B knockdown inhibits radiation-induced PKC integrated integrin signaling to the cytoskeleton of glioma-initiating cells. International Journal of Oncology, 41, 599-610. https://doi.org/10.3892/ijo.2012.1496
MLA
Alapati, K., Gopinath, S., Malla, R. R., Dasari, V. R., Rao, J. S."uPAR and cathepsin B knockdown inhibits radiation-induced PKC integrated integrin signaling to the cytoskeleton of glioma-initiating cells". International Journal of Oncology 41.2 (2012): 599-610.
Chicago
Alapati, K., Gopinath, S., Malla, R. R., Dasari, V. R., Rao, J. S."uPAR and cathepsin B knockdown inhibits radiation-induced PKC integrated integrin signaling to the cytoskeleton of glioma-initiating cells". International Journal of Oncology 41, no. 2 (2012): 599-610. https://doi.org/10.3892/ijo.2012.1496
Copy and paste a formatted citation
x
Spandidos Publications style
Alapati K, Gopinath S, Malla RR, Dasari VR and Rao JS: uPAR and cathepsin B knockdown inhibits radiation-induced PKC integrated integrin signaling to the cytoskeleton of glioma-initiating cells. Int J Oncol 41: 599-610, 2012.
APA
Alapati, K., Gopinath, S., Malla, R.R., Dasari, V.R., & Rao, J.S. (2012). uPAR and cathepsin B knockdown inhibits radiation-induced PKC integrated integrin signaling to the cytoskeleton of glioma-initiating cells. International Journal of Oncology, 41, 599-610. https://doi.org/10.3892/ijo.2012.1496
MLA
Alapati, K., Gopinath, S., Malla, R. R., Dasari, V. R., Rao, J. S."uPAR and cathepsin B knockdown inhibits radiation-induced PKC integrated integrin signaling to the cytoskeleton of glioma-initiating cells". International Journal of Oncology 41.2 (2012): 599-610.
Chicago
Alapati, K., Gopinath, S., Malla, R. R., Dasari, V. R., Rao, J. S."uPAR and cathepsin B knockdown inhibits radiation-induced PKC integrated integrin signaling to the cytoskeleton of glioma-initiating cells". International Journal of Oncology 41, no. 2 (2012): 599-610. https://doi.org/10.3892/ijo.2012.1496
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