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Regulation of epidermal growth factor receptor in human colon cancer cell lines by interferon α
  1. J-L Yang1,
  2. X-J Qu2,
  3. P J Russell3,
  4. D Goldstein4
  1. 1Department of Surgery, Prince of Wales Hospital, University of New South Wales, Sydney, Australia
  2. 2Department of Pharmacology, Institute of Materia Medica, Shandong Academy of Medical Sciences, Jinan, P R China
  3. 3Oncology Research Centre, Prince of Wales Hospital, University of New South Wales, Sydney, Australia
  4. 4Department of Medical Oncology, Prince of Wales Hospital, University of New South Wales, Sydney, Australia
  1. Correspondence to:
    Dr D Goldstein
    Department of Medical Oncology, Prince of Wales Hospital, Barker St, Randwick, Sydney, NSW, 2031, Australia;


Background and aim: The biology of growth factor receptor expression has implications for receptor specific cancer therapy. In this study, we examined: (a) regulation of epidermal growth factor receptor (EGFR) expression in a panel of 10 human colon cancer cell lines using interferon α (IFN-α); (b) ability of IFN-α to inhibit cell proliferation; and (c) sensitivity of IFN-α pretreated cells to EGF.

Methods: Cell proliferation was measured both by crystal violet colorimetric and clonogenic assays. Cell surface, intracellular, and/or total cell protein expression of EGFR was assessed by indirect immunofluorescence flow cytometry and/or fluorescein isothiocyanate (FITC)-EGF binding and internalisation flow cytometric assay.

Results: IFN-α treatment upregulated expression of cell surface EGFR in seven of 10 colon cancer cell lines within 16 hours, reaching a peak within 48–96 hours; this was accompanied by transient elevation of intracellular EGFR and marked growth inhibition. IFN-α treated cancer cells were still sensitive to EGF proliferative stimulation.

Conclusions: Our results indicate that cytostatic concentrations of IFN-α can enhance cell surface and intracellular EGFR expression in a proportion of human colon cancer cells. The antiproliferative action of IFN-α could not block the signal transduction of the EGF-EGFR pathway. This may have clinical implications for improving treatment based on targeting of EGFR.

  • Keywords: epidermal growth factor
  • epidermal growth factor receptor
  • interferon α
  • colon cancer
  • cell lines
  • EGF, epidermal growth factor
  • EGFR, epidermal growth factor receptor
  • IFN-α, interferon α
  • FCS, fetal calf serum
  • PBS, phosphate buffered saline
  • FITC, fluorescein isothiocyanate
  • MFI, mean fluorescence intensity
  • IFNαR1, interferon α receptor 1
  • IFNαR2, interferon α receptor 2
  • JAK, Janus kinases
  • STAT, signalling transducers and activators of transcription
  • IRF-1, interferon regulatory factor 1
  • MAPK, stress dependent mitogen activator protein kinase

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