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Novel estrogen and tamoxifen induced genes identified by SAGE (Serial Analysis of Gene Expression)

Abstract

The breast cancer promoting effects of estrogen and the chemopreventive effects of tamoxifen are thought to be mediated by the estrogen receptor, a ligand-dependent transcription factor. Therefore, comprehensive analysis of gene expression profiles following estrogen or tamoxifen treatment may help us better understand the role estrogen plays in tumorigenesis. We utilized SAGE (Serial Analysis of Gene Expression) technology to identify genes regulated by estrogen and tamoxifen in the ZR75-1 estrogen dependent breast cancer cell line. In this manner we have identified several genes that were regulated by estrogen or tamoxifen. Here we report the identification and initial characterization of EIT-6 (Estrogen Induced Tag-6), a novel nuclear protein and a new member of the evolutionarily conserved SM-20 family of growth regulatory immediate-early genes. EIT-6 appears to be a direct transcriptional target of the estrogen receptor and constitutive expression of EIT-6 promotes colony growth in human breast cancer cells. These data indicate that EIT-6 may play a role in estrogen induced cell growth.

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Acknowledgements

We thank Carmen Tam and Massimo Loda for mRNA in situ hybridization. Jim DiRenzo and Yongfeng Shang for helpful advice with luciferase assays. Danielle Garneau and Ed Fox for sequencing the SAGE libraries, Bill Sellers, Myles Brown, and Alexander Miron for critical review of the manuscript. This work was, in part, supported by the Sydney Kimmel Cancer Foundation (K Polyak), a US department of Defense postdoctoral fellowship (DAMD17-01-1-0221) to P Seth and the Dana-Farber Cancer Institute.

Accession number The GenBank accession number for the human EIT-6 cDNA sequence reported in this paper is AY040565.

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Correspondence to Kornelia Polyak.

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Seth, P., Krop, I., Porter, D. et al. Novel estrogen and tamoxifen induced genes identified by SAGE (Serial Analysis of Gene Expression). Oncogene 21, 836–843 (2002). https://doi.org/10.1038/sj.onc.1205113

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