STAT1 and Nmi are downstream targets of Ets-1 transcription factor in MCF-7 human breast cancer cell

Hae Hyun Jung; Jeeyun Lee; Joo Hyun Kim; Kyoung-Ju Ryu; Sun-A Kang; Chaehwa Park; Kiwoong Sung; Do-Hyun Nam; Won Ki Kang; Keunchil Park; Young-Hyuck Im

doi:10.1016/j.febslet.2005.06.011

STAT1 and Nmi are downstream targets of Ets-1 transcription factor in MCF-7 human breast cancer cell

FEBS Lett. 2005 Jul 18;579(18):3941-6. doi: 10.1016/j.febslet.2005.06.011.

Authors

Hae Hyun Jung¹, Jeeyun Lee, Joo Hyun Kim, Kyoung-Ju Ryu, Sun-A Kang, Chaehwa Park, Kiwoong Sung, Do-Hyun Nam, Won Ki Kang, Keunchil Park, Young-Hyuck Im

Affiliation

¹ Biomedical Research Institute, Samsung Medical Center, Sungkyunkwan University School of Medicine, 50 Ilwon-dong Kangnam-gu, Seoul 135-710, Korea.

PMID: 15996661
DOI: 10.1016/j.febslet.2005.06.011

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.

Publication types

Research Support, Non-U.S. Gov't

MeSH terms

Actins / metabolism
Apoptosis
Blotting, Western
Breast Neoplasms / metabolism*
Cell Differentiation
Cell Line, Tumor
Cell Proliferation
DNA, Complementary / metabolism
DNA-Binding Proteins / metabolism*
Down-Regulation
Gene Expression Regulation, Neoplastic*
Humans
Intracellular Signaling Peptides and Proteins / metabolism*
Neovascularization, Pathologic
Oligonucleotide Array Sequence Analysis
Proto-Oncogene Protein c-ets-1
Proto-Oncogene Proteins / metabolism*
Proto-Oncogene Proteins c-ets
RNA / metabolism
RNA, Messenger / metabolism
RNA, Small Interfering / metabolism
Reverse Transcriptase Polymerase Chain Reaction
STAT1 Transcription Factor
Time Factors
Trans-Activators / metabolism*
Transcription Factors / metabolism*
Transfection

Substances

Actins
DNA, Complementary
DNA-Binding Proteins
ETS1 protein, human
Intracellular Signaling Peptides and Proteins
NMI protein, human
Proto-Oncogene Protein c-ets-1
Proto-Oncogene Proteins
Proto-Oncogene Proteins c-ets
RNA, Messenger
RNA, Small Interfering
STAT1 Transcription Factor
STAT1 protein, human
Trans-Activators
Transcription Factors
RNA