التفاصيل البيبلوغرافية
| العنوان: |
STAT1 and Nmi are downstream targets of Ets-1 transcription factor in MCF-7 human breast cancer cell |
| المؤلفون: |
Jung, Hae Hyun1, Lee, Jeeyun1,2, Kim, Joo Hyun1, Ryu, Kyoung-Ju1, Kang, Sun-A1, Park, Chaehwa1, Sung, Kiwoong3, Nam, Do-Hyun4, Kang, Won Ki1,2, Park, Keunchil1,2, Im, Young-Hyuck1,2 imyh@smc.samsung.co.kr |
| المصدر: |
FEBS Letters. Jul2005, Vol. 579 Issue 18, p3941-3946. 6p. |
| مصطلحات موضوعية: |
*ONCOGENES, *TRANSCRIPTION factors, *CELL proliferation, *NEOVASCULARIZATION |
| مستخلص: |
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. [Copyright &y& Elsevier] |
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