IL-4-induced Stat6 activities affect apoptosis and gene expression in breast cancer cells

Wen Jie Zhang, Ben Hui Li, Xian Zi Yang, Pin Dong Li, Qin Yuan, Xiao Hong Liu, Shuang Bing Xu, Yan Zhang, Jia Yuan, Glenn S. Gerhard, Kathryn K. Masker, Cheng Dong, Walter A. Koltun, Michael J. Chorney

Research output: Contribution to journalArticlepeer-review

54 Scopus citations


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 Stat6high phenotype and BT-20 being defective Stat6null phenotype, respectively. Breast cancer cells carrying Stat6null phenotype exhibited increased spontaneous apoptosis compared with those carrying Stat6high 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 Stat6null BT-20 cells and 23 genes unique to Stat6high ZR-75-1 cells, respectively. Furthermore, Stat6high and Stat6null 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.

Original languageEnglish (US)
Pages (from-to)39-47
Number of pages9
Issue number1
StatePublished - Apr 2008

All Science Journal Classification (ASJC) codes

  • Molecular Biology
  • Hematology
  • Biochemistry
  • Immunology and Allergy
  • Immunology


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