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Loss of STAT1 expression confers resistance to IFN‐γ‐induced apoptosis in ME180 cells
Author(s) -
Lee Kye Young,
Anderson Emily,
Madani Kamyar,
Rosen Glenn D
Publication year - 1999
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/s0014-5793(99)01283-1
Subject(s) - stat1 , stat protein , apoptosis , cell culture , biology , tumor necrosis factor alpha , interferon gamma , interferon , irf1 , transcription factor , microbiology and biotechnology , programmed cell death , stat3 , cancer research , signal transduction , cytokine , gene , immunology , biochemistry , genetics
Interferon gamma (IFN‐γ) induces apoptosis in many tumor cell lines and sensitizes tumor cells to apoptosis by tumor necrosis factor family members. IFN‐γ induces the expression of many early response genes such as interferon regulatory factor‐1 (IRF‐1) by activation of signal transducer and activator of transcription (STAT) factor proteins. We found that ME180 cells became resistant to IFN‐γ‐induced cell death after 4–5 passages in culture. These resistant cells were characterized by a loss of STAT1 expression and a loss of inducible IRF‐1 expression. We describe for the first time the emergence of a STAT1‐deficient ME180 cell line.