Interferon-γ suppresses S100A4 transcription independently of apoptosis or cell cycle arrest

被引：17

作者：

Andersen, K ^{[1
]}

Smith-Sorensen, B ^{[1
]}

Pedersen, KB ^{[1
]}

Hovig, E ^{[1
]}

Myklebost, O ^{[1
]}

Fodstad, O ^{[1
]}

Mælandsmo, GM ^{[1
]}

机构：

[1] Norwegian Radium Hosp, Dept Tumor Biol, N-0310 Oslo, Norway

来源：

BRITISH JOURNAL OF CANCER | 2003年 / 88卷 / 12期

关键词：

mammary carcinoma; colon carcinoma; osteosarcoma; Jak-STAT1; signalling; microarray;

D O I：

10.1038/sj.bjc.6600998

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 ;

摘要：

The S100A4 protein has been associated with increased metastatic capacity of cancer cells, and recent studies have suggested a correlation between the expression level of S100A4 and the prognostic outcome for patients with various types of cancer. The knowledge about the mechanisms underlying the metastasis-promoting effects is still limited, and the aim of the present study was to elucidate signal transduction pathways involved in the regulation of S100A4. After treatment of human carcinoma cells with interferon-gamma (IFN-gamma), we observed downregulation of S100A4 both at mRNA and protein levels. The effect was not dependent on IFN-gamma-induced apoptosis or IFN-gamma-mediated cell cycle arrest. Moreover, IFN-gamma-mediated decrease in mRNA stability could not account for the observed decrease in S100A4 transcript level. Finally, microarray analysis suggests ISGF3G, ETV5, ZNF133 and CEBPG as possible candidate genes involved in IFN-gamma-mediated repression of S100A4.

引用

页码：1995 / 2001

页数：7

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