Back to Search
Start Over
IL-4-induced Stat6 activities affect apoptosis and gene expression in breast cancer cells.
- Source :
-
Cytokine [Cytokine] 2008 Apr; Vol. 42 (1), pp. 39-47. Date of Electronic Publication: 2008 Mar 14. - Publication Year :
- 2008
-
Abstract
- IL-4-induced Stat6 signaling is active in a variety of cell types, including immune cells and cancer cells, and plays an important role in the regulation of gene expression. Using EMSA gel shift assay and an antibody to Stat6, we phenotyped two breast cancer cell lines, ZR-75-1 being active Stat6(high) phenotype and BT-20 being defective Stat6(null) phenotype, respectively. Breast cancer cells carrying Stat6(null) phenotype exhibited increased spontaneous apoptosis compared with those carrying Stat6(high) phenotype. Expression microarray analyses demonstrated that IL-4 upregulated CCL26, SOCS1, CISH, EGLN3, and SIDT1, and downregulated DUSP1, FOS, and FOSB, respectively, in these breast cancer cells. Among those genes, CCL26 and SOCS1 were known genes regulated by IL-4/Stat6 pathway, but CISH, EGLN3, SIDT1, DUSP1, FOS, and FOSB were novel genes demonstrated to be IL-4 responsive for the first time. IL-4 also upregulated 38 genes unique to Stat6(null) BT-20 cells and 23 genes unique to Stat6(high) ZR-75-1 cells, respectively. Furthermore, Stat6(high) and Stat6(null) cells showed very different profiles of constitutively expressed genes relevant to apoptosis and metastasis among others, which serve as a valuable expression database and warrant for detailed studies of IL-4/Stat6 pathway in breast cancer.
- Subjects :
- Cell Line, Tumor
Female
Gene Expression Profiling
Humans
Interleukin-4 genetics
Molecular Sequence Data
Neoplasm Metastasis
Oligonucleotide Array Sequence Analysis
Phenotype
Reproducibility of Results
STAT6 Transcription Factor genetics
Apoptosis physiology
Breast Neoplasms metabolism
Gene Expression Regulation
Interleukin-4 metabolism
STAT6 Transcription Factor metabolism
Signal Transduction physiology
Subjects
Details
- Language :
- English
- ISSN :
- 1096-0023
- Volume :
- 42
- Issue :
- 1
- Database :
- MEDLINE
- Journal :
- Cytokine
- Publication Type :
- Academic Journal
- Accession number :
- 18342537
- Full Text :
- https://doi.org/10.1016/j.cyto.2008.01.016