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Oncology Reports
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Print ISSN: 1021-335X Online ISSN: 1791-2431
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June 2006 Volume 15 Issue 6

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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.

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Medicine International

An International Open Access Journal Devoted to General Medicine.

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Article

siRNA mediated knockdown of fibroblast growth factor receptors 1 or 3 inhibits FGF-induced anchorage-independent clonogenicity but does not affect MAPK activation

  • Authors:
    • Norman R. Estes II
    • Jaideep V. Thottassery
    • Francis G. Kern

  • View Affiliations / Copyright

    Affiliations: Biochemistry and Molecular Biology Department, Drug Discovery Division, Southern Research Institute, 2000 Ninth Avenue South, Birmingham, AL 35255, USA
  • Pages: 1407-1416
    |
    Published online on: June 1, 2006
       https://doi.org/10.3892/or.15.6.1407
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Abstract

Supplementation with exogenous growth factors such as fibroblast growth factors (FGFs) is essential for anchorage-independent growth of the SW-13 human adrenal adenocarcinoma cell line. We have found that SW-13 cells express mRNAs for FGFRs 1, 3, and 4, but not FGFR2. To assess the roles of individual FGFRs, in anchorage-independent growth, we determined the effects of down-regulation of each FGFR on FGF2- and FGF4-mediated soft agar colony formation in these cells. Using RNAi strategies we found that knockdown of either FGFR1 or FGFR3 leads to inhibition of FGF2- or FGF4-induced soft agar clonogenicity without affecting that induced by heregulin β1. However, this inhibition is independent of ERK1/2 activation as levels of FGF-induced phospho-ERK 1/2 remain unchanged upon knockdown of either FGFR1 or FGFR3. Conversely, RNAi-mediated knockdown of FGFR4 appeared to have no significant effect on either FGF2- or FGF4-induced anchorage-independent colony formation, or ERK1/2 phosphorylation. These results suggest that constitutive levels of both FGFR1 and FGFR3, but not FGFR4 are essential for FGF-stimulated anchorage-independent growth of SW-13 cells.

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Copy and paste a formatted citation
Spandidos Publications style
Estes II NR, Thottassery JV and Kern FG: siRNA mediated knockdown of fibroblast growth factor receptors 1 or 3 inhibits FGF-induced anchorage-independent clonogenicity but does not affect MAPK activation. Oncol Rep 15: 1407-1416, 2006.
APA
Estes II, N.R., Thottassery, J.V., & Kern, F.G. (2006). siRNA mediated knockdown of fibroblast growth factor receptors 1 or 3 inhibits FGF-induced anchorage-independent clonogenicity but does not affect MAPK activation. Oncology Reports, 15, 1407-1416. https://doi.org/10.3892/or.15.6.1407
MLA
Estes II, N. R., Thottassery, J. V., Kern, F. G."siRNA mediated knockdown of fibroblast growth factor receptors 1 or 3 inhibits FGF-induced anchorage-independent clonogenicity but does not affect MAPK activation". Oncology Reports 15.6 (2006): 1407-1416.
Chicago
Estes II, N. R., Thottassery, J. V., Kern, F. G."siRNA mediated knockdown of fibroblast growth factor receptors 1 or 3 inhibits FGF-induced anchorage-independent clonogenicity but does not affect MAPK activation". Oncology Reports 15, no. 6 (2006): 1407-1416. https://doi.org/10.3892/or.15.6.1407
Copy and paste a formatted citation
x
Spandidos Publications style
Estes II NR, Thottassery JV and Kern FG: siRNA mediated knockdown of fibroblast growth factor receptors 1 or 3 inhibits FGF-induced anchorage-independent clonogenicity but does not affect MAPK activation. Oncol Rep 15: 1407-1416, 2006.
APA
Estes II, N.R., Thottassery, J.V., & Kern, F.G. (2006). siRNA mediated knockdown of fibroblast growth factor receptors 1 or 3 inhibits FGF-induced anchorage-independent clonogenicity but does not affect MAPK activation. Oncology Reports, 15, 1407-1416. https://doi.org/10.3892/or.15.6.1407
MLA
Estes II, N. R., Thottassery, J. V., Kern, F. G."siRNA mediated knockdown of fibroblast growth factor receptors 1 or 3 inhibits FGF-induced anchorage-independent clonogenicity but does not affect MAPK activation". Oncology Reports 15.6 (2006): 1407-1416.
Chicago
Estes II, N. R., Thottassery, J. V., Kern, F. G."siRNA mediated knockdown of fibroblast growth factor receptors 1 or 3 inhibits FGF-induced anchorage-independent clonogenicity but does not affect MAPK activation". Oncology Reports 15, no. 6 (2006): 1407-1416. https://doi.org/10.3892/or.15.6.1407
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