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Cancer Res. 1995 Sep 15;55(18):4099-104.

Interferon system defects in human malignant melanoma.

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Biology Division, Wellcome Foundation Ltd., Beckenham, Kent, United Kingdom.


We have examined the ability of melanoma cell lines and normal human melanocytes, which have demonstrable intact IFN genes, to secrete both IFN-alpha and IFN-beta in response to induction with virus. Normal melanocytes were found to secrete both IFN-alpha and IFN-beta after virus induction. In contrast, although all but one of the melanoma lines tested were capable of secreting IFN-beta, none were capable of IFN-alpha secretion. This phenomenon was not due to defects in either translation of IFN-alpha mRNA or secretion of IFN-alpha proteins, since transfection of melanoma lines with a constitutive IFN-alpha 2b expression vector resulted in the secretion of high levels of IFN. On further examination, this inability to express natural IFN-alpha appeared to be due to a defect in activation of the IFN-alpha promoters, since constructs containing the IFN-alpha promotor were completely unresponsive to viral infection in melanoma cells but inducible in melanocytes. These results show that there is a specific disruption of IFN-alpha gene activation rather than IFN-beta in melanoma lines and suggest that this is due to disruption of a trans-acting IFN-alpha gene transcription factor. Disruption of this factor and its consequences may be important in the development of malignant melanoma.

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