The molecular biology and nomenclature of the activating transcription factor/cAMP responsive element binding family of transcription factors: activating transcription factor proteins and homeostasis

Hai, Tsonwin; Hartman, Matthew G.

doi:10.1016/s0378-1119(01)00551-0

Cited by 733 publications

(675 citation statements)

References 87 publications

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“…Overwhelming evidence indicates that the ATF3 mRNA level is not detectable in most cells, but greatly increased by a variety of stress signals, including anoxia (Ameri et al, 2007), hypoxia, DNA damage and carcinogens (Hai et al, 1999;Hai and Hartman, 2001). However, recent literature indicates that some of the signals that can induce ATF3 gene expression do not fit the conventional definition of stress signals (Hai, 2006).…”

Section: Introductionmentioning

confidence: 99%

A potential dichotomous role of ATF3, an adaptive-response gene, in cancer development

2007

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Activating transcription factor 3 (ATF3) is a member of the ATF/cyclic AMP response element-binding family of transcription factors. We present evidence that ATF3 has a dichotomous role in cancer development. By both gain-and loss-of-function approaches, we found that ATF3 enhances apoptosis in the untransformed MCF10A mammary epithelial cells, but protects the aggressive MCF10CA1a cells and enhances its cell motility. Array analyses indicated that ATF3 upregulates the expression of several genes in the tumor necrosis factor pathway in the MCF10A cells but upregulates the expression of several genes implicated in tumor metastasis, including TWIST1, fibronectin (FN)-1, plasminogen activator inhibitor-1, urokinase-type plasminogen activator, caveolin-1 and Slug, in the MCF10CA1a cells. We present evidence that ATF3 binds to the endogenous promoters and regulates the transcription of the TWIST1, FN-1, Snail and Slug genes. Furthermore, conditioned medium experiments indicated that ATF3 has a paracrine/autocrine effect, consistent with its upregulation of genes encoding secreted factors. Finally, ATF3 gene copy number is >2 in B80% of the breast tumors examined (N ¼ 48) and its protein level is elevated in B50% of the tumors. These results provided a correlative argument that it is advantageous for the malignant cancer cells to express ATF3, consistent with its oncogenic roles suggested by the MCF10CA1a cell data.

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Section: Introductionmentioning

confidence: 99%

A potential dichotomous role of ATF3, an adaptive-response gene, in cancer development

2007

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“…ATF3 has been suggested to be critical in metastasis, and has also been reported to be proapoptotic as well as antiapoptotic (Ishiguro and Nagawa, 2000;Hai and Hartman, 2001;Francis et al, 2004;Hartman et al, 2004). As this paper was Anoxic induction of ATF3 K Ameri et al completed, it was reported that ATF3 stabilizes p53 upon genotoxic stress (Yan et al, 2005), and also induces tubulogenic differentiation in endothelial cells and angiogenesis in diabetic angiopathy (Okamoto et al, 2006).…”

mentioning

confidence: 82%

“…First, ATF3 is induced by a variety of stress signals (Hai et al, 1999). Second, expression of ATF3 has been demonstrated to alter a variety of cellular processes relevant to cancer progression including cell cycle, cell death, angiogenesis and metastasis (Hai and Hartman, 2001;Okamoto et al, 2006). Third, ATF3 expression can be regulated transcriptionally by a variety of signalling pathways or transcription factors, including nuclear factor kappa B (Hartman et al, 2004), EGR-1 (Bottone et al, 2005), by p53-dependent and -independent pathways (Amundson et al, 1999;Fan et al, 2002), and by the c-Jun NH 2 -terminal kinase (JNK) (Cai et al, 2000), which is activated by MKK7 (Tournier et al, 1997).…”

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confidence: 99%

Induction of activating transcription factor 3 by anoxia is independent of p53 and the hypoxic HIF signalling pathway

et al. 2006

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Solid tumors often have an inadequate blood supply, which results in large regions that are subjected to hypoxic or anoxic stress. Hypoxia-inducible factor-1 (HIF-1) is a transcription factor that regulates much of the transcriptional response of cells to hypoxia. Activating transcription factor 3 (ATF3) is another transcription factor that responds to a variety of stresses and is often upregulated in cancer. We investigated the regulation of ATF3 by oxygen deprivation. ATF3 induction occurred most robustly under anoxia, is common, and it is not dependent on presence of HIF-1 or p53, but is sensitive to the inhibition of c-Jun NH2-terminal kinase activation and the antioxidant N-acetylcystein. ATF3 could also be induced by desferrioxamine but not by the mitochondrial poison cyanide or the nonspecific 2-oxoglutarate dioxygenase inhibitor dimethyloxalylglycine. We also show that anoxic ATF3 mRNA is more stable than normoxic mRNA providing a mechanism for this induction. Thus, this study demonstrates that the regulation of ATF3 under anoxia is independent of 2-oxoglutarate dioxygenase, HIF-1 and p53, presumably involving multiple regulatory pathways.

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“…It is known that ATF-3 regulates gene expression through dimerizing or interacting with other transcription factors in the leucine zipper family like Fos/Jun [35,36], which allows binding to Ap1 and CRE/ATF promoters [37,38]. Upon injury, ATF-3 is upregulated in many neurons in the CNS [39,40] and peripheral nervous system [41,42].…”

Section: Transcription Factor Involvement In Dendritic Plasticitymentioning

confidence: 99%

“…Upon overexpression, ATF-3 stimulates enhanced neurite outgrowth in vitro, suggesting that the transcription factor increases growth plasticity in neurons, although the exact transcriptional mechanism remains unclear. Some genes regulated by ATF-3 in neuronal cells include heat shock protein 27 (Hsp27) [43] and c-Jun [38], the latter of which is involved in ATF-3-mediated neurite growth [44]. It could be that ATF-3 acts in concert with other transcription factors and modulates the expression of various genes to stimulate such neuronal responses.…”

Section: Transcription Factor Involvement In Dendritic Plasticitymentioning

confidence: 99%

Transcriptional and Epigenetic Regulation in Injury-Mediated Neuronal Dendritic Plasticity

Wang

et al. 2016

Neurosci. Bull.

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Injury to the nervous system induces localized damage in neural structures and neuronal death through the primary insult, as well as delayed atrophy and impaired plasticity of the delicate dendritic fields necessary for interneuronal communication. Excitotoxicity and other secondary biochemical events contribute to morphological changes in neurons following injury. Evidence suggests that various transcription factors are involved in the dendritic response to injury and potential therapies. Transcription factors play critical roles in the intracellular regulation of neuronal morphological plasticity and dendritic growth and patterning. Mounting evidence supports a crucial role for epigenetic modifications via histone deacetylases, histone acetyltransferases, and DNA methyltransferases that modify gene expression in neuronal injury and repair processes. Gene regulation through epigenetic modification is of great interest in neurotrauma research, and an early picture is beginning to emerge concerning how injury triggers intracellular events that modulate such responses. This review provides an overview of injury-mediated influences on transcriptional regulation through epigenetic modification, the intracellular processes involved in the morphological consequences of such changes, and potential approaches to the therapeutic manipulation of neuronal epigenetics for regulating gene expression to facilitate growth and signaling through dendritic arborization following injury.

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The molecular biology and nomenclature of the activating transcription factor/cAMP responsive element binding family of transcription factors: activating transcription factor proteins and homeostasis

Cited by 733 publications

References 87 publications

A potential dichotomous role of ATF3, an adaptive-response gene, in cancer development

A potential dichotomous role of ATF3, an adaptive-response gene, in cancer development

Induction of activating transcription factor 3 by anoxia is independent of p53 and the hypoxic HIF signalling pathway

Transcriptional and Epigenetic Regulation in Injury-Mediated Neuronal Dendritic Plasticity

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