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(Received for publication, November 26, 1997, and in revised form, June 25, 1997)
From the The mechanism of IFN resistance was examined in
three long-term cell lines, SK-MEL-28, SK-MEL-3, and MM96, exhibiting
significant variation in responsiveness to the antiproliferative and
antiviral effects of type I IFNs. The JAK-STAT components involved in
IFN signal transduction were analyzed in detail. After exposure to IFN,
activation of the IFN type I receptor-linked tyrosine kinases, JAK-1
and TYK-2, was detected at similar levels in both IFN-sensitive and
IFN-resistant cell types, indicating that IFN resistance did not result
from a deficiency in signaling at the level of receptor-associated kinase activation. However, analysis of ISGF3 transcription factor components, STAT1, STAT2, and p48-ISGF3
Volume 272, Number 45,
Issue of November 7, 1997
pp. 28779-28785
©1997 by The American Society for Biochemistry and Molecular Biology, Inc.
Interferon-resistant Human Melanoma Cells Are Deficient in ISGF3
Components, STAT1, STAT2, and p48-ISGF3
,
,
,
,
and
Department of Biochemistry and Molecular
Biology, Monash University, Wellington Road, Clayton, Victoria 3168, Australia, § Immunology and Oncology Unit, John Hunter
Hospital, Newcastle, New South Wales 2300, Australia, and ¶ Centre
for Hormone Research, Royal Children's Hospital,
Parkville, Victoria 3052, Australia
, revealed that their expression and activation correlated with cellular IFN responsiveness. The analysis was extended to also include IFN-sensitive primary melanocytes, three additional IFN-resistant melanoma cell lines, and
seven cell cultures recently established from melanoma patient biopsies. It was consistently observed that the most marked difference in ISGF3 was a lack of STAT1 in the resistant versus the
sensitive cells. Transfection of the IFN-resistant MM96 cell line to
express increased levels of STAT1 protein partially restored IFN
responsiveness in an antiviral assay. We conclude that a defect in the
level of STAT1 and possibly all three ISGF3 components in IFN-resistant human melanoma cells may be a general phenomenon responsible for reduced cellular responsiveness of melanomas to IFNs.
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