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Research Article Free access | 10.1172/JCI113861

Interferons modulate the expression of hormone receptors on the surface of murine melanoma cells.

K Kameyama, S Tanaka, Y Ishida, and V J Hearing

Laboratory of Cell Biology, National Cancer Institute, Bethesda, Maryland.

Find articles by Kameyama, K. in: PubMed | Google Scholar

Laboratory of Cell Biology, National Cancer Institute, Bethesda, Maryland.

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Laboratory of Cell Biology, National Cancer Institute, Bethesda, Maryland.

Find articles by Ishida, Y. in: PubMed | Google Scholar

Laboratory of Cell Biology, National Cancer Institute, Bethesda, Maryland.

Find articles by Hearing, V. in: PubMed | Google Scholar

Published January 1, 1989 - More info

Published in Volume 83, Issue 1 on January 1, 1989
J Clin Invest. 1989;83(1):213–221. https://doi.org/10.1172/JCI113861.
© 1989 The American Society for Clinical Investigation
Published January 1, 1989 - Version history
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Abstract

The effects of IFN-alpha, IFN-beta, and IFN-gamma on the differentiation of murine melanoma cells has been studied, in the presence and absence of melanocyte-stimulating hormone (MSH); the cells were highly responsive to treatment with MSH, which increased the rate of melanin production 25-fold and tyrosinase activity 6-fold within 4 d. Treatment of melanoma cells with IFN-alpha, IFN-beta, or IFN-gamma alone had no stimulatory effect on melanin production, but when the cells were cultured with IFN in the presence of MSH, pigment production was significantly and synergistically increased relative to cells cultured with MSH only. Flow cytometric analysis revealed that levels of tyrosinase in the cells were not affected by MSH or by IFN, which suggests that stimulation of melanogenic activity occurred by activation of a preexisting cellular enzyme. Scatchard analyses showed that the number of MSH receptors on IFN-treated cells was significantly increased (approximately 2.5-fold) relative to untreated cells (approximately 61,000/cell). These findings demonstrate that IFN stimulate differentiation (that is, pigmentation) of melanocytes by increasing the expression of surface MSH receptors; this in turn suggests that such a mechanism may in part be responsible for postinflammatory skin pigmentation, and provides an additional basis for action in the clinical responses of melanoma to IFN treatment.

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