Gene expression regulated by IL-4/ Stat6 signaling pathway in breast cancer cells with different Stat6 activation phenotypes

Ben Hui Li, Xian Zi Yang, Pin Dong Li, Qin Yuan, Xiao Hong Liu, Glenn S. Gerhard, Cheng Dong, Michael J. Chorney, Wen Jie Zhang

Research output: Contribution to journalArticle

Abstract

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 languageEnglish (US)
Pages (from-to)161-163
Number of pages3
JournalChinese Journal of Cancer Prevention and Treatment
Volume16
Issue number3
StatePublished - Feb 1 2009

Fingerprint

Interleukin-4
Breast Neoplasms
Phenotype
Gene Expression
Apoptosis
Genes
Human Genome
Flow Cytometry
Neoplasm Metastasis

All Science Journal Classification (ASJC) codes

  • Oncology

Cite this

Li, B. H., Yang, X. Z., Li, P. D., Yuan, Q., Liu, X. H., Gerhard, G. S., ... Zhang, W. J. (2009). Gene expression regulated by IL-4/ Stat6 signaling pathway in breast cancer cells with different Stat6 activation phenotypes. Chinese Journal of Cancer Prevention and Treatment, 16(3), 161-163.
Li, Ben Hui ; Yang, Xian Zi ; Li, Pin Dong ; Yuan, Qin ; Liu, Xiao Hong ; Gerhard, Glenn S. ; Dong, Cheng ; Chorney, Michael J. ; Zhang, Wen Jie. / Gene expression regulated by IL-4/ Stat6 signaling pathway in breast cancer cells with different Stat6 activation phenotypes. In: Chinese Journal of Cancer Prevention and Treatment. 2009 ; Vol. 16, No. 3. pp. 161-163.
@article{a7fe23d7c0ef423680d7cfe94a7ee817,
title = "Gene expression regulated by IL-4/ Stat6 signaling pathway in breast cancer cells with different Stat6 activation phenotypes",
abstract = "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.",
author = "Li, {Ben Hui} and Yang, {Xian Zi} and Li, {Pin Dong} and Qin Yuan and Liu, {Xiao Hong} and Gerhard, {Glenn S.} and Cheng Dong and Chorney, {Michael J.} and Zhang, {Wen Jie}",
year = "2009",
month = "2",
day = "1",
language = "English (US)",
volume = "16",
pages = "161--163",
journal = "Chinese Journal of Cancer Prevention and Treatment",
issn = "1673-5269",
publisher = "Chinese Journal of Cancer Prevention and Treatment, Editorial board",
number = "3",

}

Gene expression regulated by IL-4/ Stat6 signaling pathway in breast cancer cells with different Stat6 activation phenotypes. / Li, Ben Hui; Yang, Xian Zi; Li, Pin Dong; Yuan, Qin; Liu, Xiao Hong; Gerhard, Glenn S.; Dong, Cheng; Chorney, Michael J.; Zhang, Wen Jie.

In: Chinese Journal of Cancer Prevention and Treatment, Vol. 16, No. 3, 01.02.2009, p. 161-163.

Research output: Contribution to journalArticle

TY - JOUR

T1 - Gene expression regulated by IL-4/ Stat6 signaling pathway in breast cancer cells with different Stat6 activation phenotypes

AU - Li, Ben Hui

AU - Yang, Xian Zi

AU - Li, Pin Dong

AU - Yuan, Qin

AU - Liu, Xiao Hong

AU - Gerhard, Glenn S.

AU - Dong, Cheng

AU - Chorney, Michael J.

AU - Zhang, Wen Jie

PY - 2009/2/1

Y1 - 2009/2/1

N2 - 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.

AB - 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.

UR - http://www.scopus.com/inward/record.url?scp=77953472157&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=77953472157&partnerID=8YFLogxK

M3 - Article

AN - SCOPUS:77953472157

VL - 16

SP - 161

EP - 163

JO - Chinese Journal of Cancer Prevention and Treatment

JF - Chinese Journal of Cancer Prevention and Treatment

SN - 1673-5269

IS - 3

ER -