IFN-γ induces cell growth inhibition by fas-mediated apoptosis: Requirement of STAT1 protein for up-regulation of Fas and FasL expression

Xiulong Xu, Xin Yuan Fu, Janet Plate, Anita S F Chong

Research output: Contribution to journalArticle

224 Citations (Scopus)

Abstract

The mechanism by which IFN-γ inhibits tumor cell growth has not been fully understood. Here we report that IFN-γ up-regulated the expression of Fas and Fas ligand (FasL) on HT29 cells, a human colon adenocarcinoma cell line, and subsequently induced apoptosis of these cells. The kinetics of cell death in IFN-γ-treated HT29 cells paralleled the increase in the levels of Fas and FasL expression. We further show that IFN-γ up-regulated the expression of Fas and FasL in STAT1-transfected U3A cells but not in STAT1- deficient U3A cells. Correspondingly, IFN-γ induced cell death in STAT1- transfected U3A cells but not in STAT1-deficient U3A cells. IFN-γ-induced cell death was inhibited by caspase-1 inhibitors. Our results suggest that cell growth inhibition by IFN-γ is due to apoptosis mediated by Fas and FasL interaction.

Original languageEnglish (US)
Pages (from-to)2832-2837
Number of pages6
JournalCancer Research
Volume58
Issue number13
StatePublished - Jul 1 1998
Externally publishedYes

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STAT1 Transcription Factor
Fas Ligand Protein
Up-Regulation
Apoptosis
Growth
HT29 Cells
Cell Death
Colon
Adenocarcinoma
Cell Line

ASJC Scopus subject areas

  • Cancer Research
  • Oncology

Cite this

IFN-γ induces cell growth inhibition by fas-mediated apoptosis : Requirement of STAT1 protein for up-regulation of Fas and FasL expression. / Xu, Xiulong; Fu, Xin Yuan; Plate, Janet; Chong, Anita S F.

In: Cancer Research, Vol. 58, No. 13, 01.07.1998, p. 2832-2837.

Research output: Contribution to journalArticle

Xu, Xiulong ; Fu, Xin Yuan ; Plate, Janet ; Chong, Anita S F. / IFN-γ induces cell growth inhibition by fas-mediated apoptosis : Requirement of STAT1 protein for up-regulation of Fas and FasL expression. In: Cancer Research. 1998 ; Vol. 58, No. 13. pp. 2832-2837.
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