The c-ets proto-oncogenes encode transcription factors that cooperate with c-Fos and c-Jun for transcriptional activation

Wasylyk, Bohdan; Wasylyk, Christine; Flores, P.; Bégué, Agnès; Leprince, Dominique; Stéhelin, D

doi:10.1038/346191a0

Cited by 479 publications

(299 citation statements)

References 18 publications

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“…Binding to E74ml, a mutant E74 oligonucleotide, was virtually undetectable (lane 2). E74ml contains a GGAA?AGAA substitution in the core of the ETS recognition site, which we and others have previously shown to obliterate the binding of ETS factors (Wasylyk et al, 1990;Nye et al, 1992;Thomas et al, 1995Thomas et al, , 1997. ELF3 also binds to a weaker ETS-binding site from the GM-CSF promoter (GM ± lane 4), but not to an AGAA mutant of this oligonucleotide (GMml ± lane 5).…”

Section: Elf3 Displays Sequence Speci®c Binding To Oligonucleotides Cmentioning

confidence: 84%

A novel epithelial-expressed ETS gene, ELF3: human and murine cDNA sequences, murine genomic organization, human mapping to 1q32.2 and expression in tissues and cancer

et al. 1997

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The ETS family of genes are implicated in cancers such as Ewings sarcoma, acute myeloid leukemia and chronic myelomoncytic leukemia. Further, they have important functions in embryonic development. Hence, identi®ca-tion and characterization of members of this family are important. We identify a novel ETS family member, ELF3, and report its human and murine cDNA sequences. The mouse cDNA has an alternatively spliced transcript with an extra 60 bp inserted. Hence we present the organization of the murine Elf3 gene together with its exon/intron structure. This gene consists of 9 exons and 8 introns spanning 4.8 kb. ELF3 binds and transactivates ETS sequences and interestingly also shows the ability to bind a GGAT-like purine core, a preferential ETS1/ETS2 type binding site. The expression of ELF3, unlike most other ETS family members, is absent in hematopoietic cells and hematopoietic organs in humans and mice. Intriguingly, the gene is speci®cally expressed in cell lines of epithelial origin and in organs such as lung, stomach, intestine, kidney that have specialized epithelial cells. We localize the human gene to 1q32.2, a region that is ampli®ed in epithelial tumors of the breast, lung and prostate. Finally, we show that ELF3 expression is increased in a lung carcinoma and adenocarcinoma, as compared to normal tissue. ELF3 is also expressed in cell lines derived from lung cancers. These results suggest that this novel ETS gene may be involved in lung tumorigenesis.

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Section: Elf3 Displays Sequence Speci®c Binding To Oligonucleotides Cmentioning

confidence: 84%

A novel epithelial-expressed ETS gene, ELF3: human and murine cDNA sequences, murine genomic organization, human mapping to 1q32.2 and expression in tissues and cancer

et al. 1997

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“…However, PU.1-transfected HT1080 cells expressed similar levels of N-ras mRNA to the parental cells and mock transfectants ( Figure 3A and B). As a member of the Ets family proteins is one of the nuclear targets of the ras signalling pathway to activate rasresponsive elements (Wasylyk et al, 1990;Galang et al, 1994), the ectopic expression of PU. I may perturb endogenous Ets family proteins, which mediate the ras signals crucial for maintenance of the transformed phenotypes of HT1080 cells.…”

Section: Discussionmentioning

confidence: 99%

Enhanced expression of the urokinase-type plasminogen activator gene and reduced colony formation in soft agar by ectopic expression of PU.1 in HT1080 human fibrosarcoma cells

Kondoh

Yamada²,

Kihara-Negishi³

et al. 1998

Br J Cancer

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Summary To investigate the cell biological function of PU.1, a member of the Ets family of transcription factors, a vector capable of expressing the protein was transfected into HT1080 human fibrosarcoma cells. Exogenous expression of PU.1 in HT1080 cells reduced colony-forming efficiency but stimulated cell migration in soft agar, although it did not affect cell growth in adherent culture. Expression of the urokinase-type plasminogen activator (uPA) mRNA, which is known to be correlated with cell migration and invasion, was enhanced in PU. 1 transfectants compared with mock transfectants. Run-on analysis demonstrated that uPA transcription was unaffected by PU.1, suggesting that this enhancement mainly occurs at a post-transcriptional level. On the other hand, treatment of HT1080 cells with the synthetic glucocorticoid dexamethasone (DEX; 10-7 M) significantly reduced uPA gene expression at a transcriptional level. Furthermore, DEX inhibited cell migration in soft agar without affecting cell growth. These negative effects of DEX on uPA expression and cell migration were alleviated by the expression of PU.1 in HT1080 cells, whereas expression of the N-ras oncogene, which is responsible for maintenance of the transformed phenotypes in HT1080 cells, was unaffected by PU.1 expression or DEX treatment in the cells. Our results suggest that expression of PU.1 can stimulate uPA gene expression at the post-transcriptional level, which may subsequently lead to activation of cell motility and/or reduced cell-cell adhesion, but reduces anchorage-independent growth of HT1080 cells.

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“…[17][18][19][20] The ets family of transcription factors has a DNA-binding domain in common that binds to a core GGA(A/T) DNA sequence. 21,22 In situ hybridization studies have shown that the proto-oncogene c-ets is expressed in endothelial cells at the beginning of blood vessel formation, under normal and pathological conditions. 23,24 Thus, previous reports suggest that the ets family may activate the transcription of genes encoding collagenase 1, stromelysine 1 and urokinase plasminogen activator, which are proteases involved in extracellular matrix degradation.…”

Section: Figure 3 Effect Of the Transfection Of Hgf Vector On The Vasmentioning

confidence: 99%

Angiogenesis induced by hepatocyte growth factor in non-infarcted myocardium and infarcted myocardium: up-regulation of essential transcription factor for angiogenesis, ets

et al. 2000

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The feasibility of a novel therapeutic strategy using angiogenic growth factors to expedite and/or augment collateral artery development has recently entered the realm of treatment of ischemic diseases. Hepatocyte growth factor (HGF) is a novel member of endothelium-specific growth factors whose mitogenic activity on endothelial cells is very potent. Although it has been demonstrated that HGF is a potential angiogenic growth factor in in vitro culture systems, there is no direct in vivo evidence for the angiogenic activity of HGF in physiological conditions. In this study, we hypothesized that transfection of HGF gene into infarcted myocardium could induce angiogenesis, potentially resulting in a beneficial response to hypoxia. Human HGF gene or control vector driven by the SR␣ promoter was transfected into rat myocardium by the HVJ-liposome method. Four days after in vivo transfection of human HGF gene, there was a marked increase in human immunoreactive HGF as compared with control vector (P Ͻ 0.01). In myocardium transfected with HGF vector, a significant increase in PCNA-positive endothelial cells was observed, while few PCNA-positive endothelial cells were detected in both control-vector-transfected and untreated myocardium. The number of vessels around

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The c-ets proto-oncogenes encode transcription factors that cooperate with c-Fos and c-Jun for transcriptional activation

Cited by 479 publications

References 18 publications

A novel epithelial-expressed ETS gene, ELF3: human and murine cDNA sequences, murine genomic organization, human mapping to 1q32.2 and expression in tissues and cancer

A novel epithelial-expressed ETS gene, ELF3: human and murine cDNA sequences, murine genomic organization, human mapping to 1q32.2 and expression in tissues and cancer

Enhanced expression of the urokinase-type plasminogen activator gene and reduced colony formation in soft agar by ectopic expression of PU.1 in HT1080 human fibrosarcoma cells

Angiogenesis induced by hepatocyte growth factor in non-infarcted myocardium and infarcted myocardium: up-regulation of essential transcription factor for angiogenesis, ets

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