Objective: To investigate the feasibility of different phenotype of Stat6 activity in different breast cancer lines and the mechanism of IL-4. Methods: To analyz the early apoptosis of ZR-75-1 and BT-20 by flow cytometry and constitutive expression profile by Affymetrix Human Genome U133 Plus 2.0 Array GeneChips whether being treated by IL-4 or not. Results: Cells carrying defective Stat6null phenotype exhibited increased spontaneous apoptosis versus those carrying Stat6high (40% vs 12%). Expression analyses showed that IL-4 upregulated CCL26, SOCS1, CISH, EGLN3, and SIDT1, and down-regulated DUSP1, FOS and FOSB, respectively, common to both Stat6high and Stat6null cells. CCL26 and SOCS1 were known to be regulated by IL-4 via Stat6 pathway, suggesting Stat6null cells having residual functions. Analyses of constitutive expression revealed 2 193 genes/transcripts overexpressed in Stat6null cells, and vice verse, 2 600 genes/transcripts overexpressed in Stat6high cells, respectively. Furthermore, Stat6null and Stat6high cells had very different profiles of constitutively expressed genes relevant to apoptosis and metastasis, amongst others. Conclusion: These observations suggest that, like in immune cells, IL-4 may function via Stat6-dependent and -independent pathways in breast cancer cells.
|Original language||English (US)|
|Number of pages||3|
|Journal||Chinese Journal of Cancer Prevention and Treatment|
|State||Published - Feb 2009|
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