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Title: STAT1 and Nmi are downstream targets of Ets-1 transcription factor in MCF-7 human breast cancer cell. Author: Jung HH, Lee J, Kim JH, Ryu KJ, Kang SA, Park C, Sung K, Nam DH, Kang WK, Park K, Im YH. Journal: FEBS Lett; 2005 Jul 18; 579(18):3941-6. PubMed ID: 15996661. Abstract: Ets-1 is a cellular homologue of the product of the viral ets oncogene of the E26 virus, and it functions as a tissue-specific transcription factor. It plays an important role in cell proliferation, differentiation, lymphoid cell development, transformation, angiogenesis, and apoptosis. Ets-1 controls the expression of critical genes involved in these processes by binding to ets binding sites present in the transcriptional regulatory regions. Here, we transiently overexpressed Ets-1 in MCF-7 and comprehensively searched for potential downstream targets of Ets-1 by cDNA microarray analysis. The expressions of several interferon-related genes including STAT1 and Nmi were augmented by the overexpression of Ets-1. RT-PCR and Western blotting confirmed the increase in the levels of STAT1 and Nmi mRNA and protein. In contrast, Ets-1 siRNA decreased the expression of STAT1 and Nmi proteins. As in our transient transfection experiments, stable overexpression of Ets-1, also increased the protein expression of STAT1 and Nmi in MCF-7 cells. Taken together, our results indicate that STAT1 and Nmi are downstream targets of Ets-1 in MCF-7 human breast cancer cells.[Abstract] [Full Text] [Related] [New Search]