Crosstalk between Myc and activating transcription factor 2 (ATF2): Myc prolongs the half-life and induces phosphorylation of ATF2

Miethe, Josef; Schwartz, Claudia; Wottrich, Katja; Wenning, Dorit; Klempnauer, Karl‐Heinz

doi:10.1038/sj.onc.1204966

Cited by 7 publications

(4 citation statements)

References 58 publications

(59 reference statements)

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“…ATF2 ubiquitination, facilitated by its association with non‐active JNK (Fuchs et al., 1997), is dimerization dependent (Fuchs and Ronai, 1999) and is primarily targeted at the transcriptionally active form of ATF2, (Fuchs et al., 2000) thereby providing a mechanism to limit ATF2 transcriptional output. ATF2 stability and activity could be prolonged upon its association with c‐Myc (Miethe et al., 2001). In S. pombe , a single member of the SAPK family called Sty1/Spc1/Phh1 stimulates gene expression via the Atf1 transcription factor, which is similar to the human ATF2 factor, and which binds to closely related DNA sequences.…”

Section: Atf2 – the Transcription Factormentioning

confidence: 99%

ATF2 on the double – activating transcription factor and DNA damage response protein

Bhoumik

López-Bergami

Ronai

2007

Pigment Cell Research

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SummarySignal transduction pathways play a key role in the regulation of key cellular processes, including survival and death. Growing evidence points to changes in signaling pathway that occur during skin tumor development and progression. Such changes impact the activity of downstream substrates, including transcription factors. The activating transcription factor 2 (ATF2) has been implicated in malignant and non-malignant skin tumor developments. ATF2 mediates both transcription and DNA damage control, through its phosphorylation by JNK ⁄ p38 or ATM ⁄ ATR respectively. Here, we summarize our present understanding of ATF2 regulation, function and contribution to malignant and non-malignant skin tumor development.

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Section: Atf2 – the Transcription Factormentioning

confidence: 99%

ATF2 on the double – activating transcription factor and DNA damage response protein

Bhoumik

López-Bergami

Ronai

2007

Pigment Cell Research

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“…Previous studies have demonstrated that Zn-DIGP can knock-down transcription of the c-myc oncogene 3-fold or more in cell cultures . Given the important functions of c-myc in mediating melanoma metastasis, − ,, we decided to evaluate the anti-metastatic activities of Zn-DIGP using an assay that mimics the hematogenous spread of malignant melanoma in vivo . C57BL/6 mice were intravenously injected into the tail vein with B16F10 cells, and after 20 days the animals were sacrificed and the number of lung metastases determined by visual inspection.…”

Section: Resultsmentioning

confidence: 99%

“…20 The c-myc oncogene encodes for a transcription factor that, together with ATF-2, plays an important role in proliferation, differentiation, and apoptosis of melanoma. 22 Abnormal c-Myc expression can lead to tumorigenesis, 23 and the inhibition of c-Myc in mouse models causes melanoma regression. 24 Given these results, we decided to evaluate the anti-metastatic activities of GPcs in vivo.…”

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confidence: 99%

Photodynamic Agents with Anti-metastatic Activities

et al. 2013

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A new concept in multifunctional anticancer agents is demonstrated. Tetrakis-(diisopropylguanidino) zinc phthalocyanine (Zn-DIGP) exhibits excellent properties as a photodynamic therapy (PDT) agent, as well as potential anti-metastatic activities in vivo. Zn-DIGP exhibits good cellular uptake and low toxicity in the dark (EC50 > 80 M) and is well tolerated upon its intravenous injection into mice at 8 mg/kg. Upon photoexcitation with red laser light (660 nm), Zn-DIGP exhibits a high quantum yield for singlet oxygen formation (Φ 0.51) that results in potent phototoxicity to cell cultures (EC50 0.16 M). Zn-DIGP is also capable of inhibiting the formation of tumor colonies in the lungs of C57BL/6 mice injected with B16F10 cells. Zn-DIGP therefore inhibits cancer growth by both lightdependent and light-independent pathways. The anti-metastatic activities of Zn-DIGP possibly result from its ability to interfere with the signaling between chemokine CXCL10 and the G protein-coupled receptor CXCR3. Zn-DIGP is a competitive inhibitor of CXCR3 activation (IC50 = 3.8 M) and selectively inhibits downstream events such as CXCL10-activated cell migration. Consistent with the presence of feedback regulation between CXCR3 binding and CXCL10 expression, Zn-DIGP causes overexpression of CXCL10. Interestingly, Zn-DIGP binds to CXCR3 without activating the receptor yet is able to cause endocytosis and degradation of this GPCR. To the best of our knowledge, Zn-DIGP is the first PDT agent that can facilitate the photodynamic treatment of primary tumors while simultaneously inhibiting the formation of metastatic tumor colonies by a light-independent mode of action. ABSTRACTA new concept in multifunctional anti-cancer agents is demonstrated. Tetrakis-(diisopropylguanidino) zinc phthalocyanine "Zn-DIGP" exhibits excellent properties as a photodynamic therapy (PDT) agent, as well as potential anti-metastatic activities in vivo. Zn-DIGP exhibits good cellular uptake and low toxicity in the dark (EC 50 > 80 µM), and is well tolerated upon its intravenous injection into mice at 8 mg / kg. Upon photoexcitation with red laser light (660 nm), Zn-DIGP exhibits a high quantum yield for singlet oxygen formation (Φ ≈ 0.51) that results in potent phototoxicity to cell cultures (EC 50 ≈ 0.16 µM). Zn-DIGP is also capable of inhibiting the formation of tumor colonies in the lungs of C57BL/6 mice injected with B16F10 cells. Zn-DIGP therefore inhibits cancer growth by both light-dependent and light-independent pathways. The anti-metastatic activities of Zn-DIGP possibly result from its ability to interfere with the signaling between chemokine CXCL10 and the G protein-coupled receptor CXCR3. Zn-DIGP is a competitive inhibitor of CXCR3 activation (IC 50 = 3.8 µM), and it selectively inhibits downstream events such as CXCL10-activated cell migration. Consistent with the presence of feedback regulation between CXCR3 binding and CXCL10 expression, Zn-DIGP causes overexpression of CXCL10. Interestingly, Zn-DIGP binds to CXCR3 without activating the...

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“…One major role of ATF2 is to regulate the response of cells to stress signals [ 47 , 48 ]. Furthermore, in 2001, Miethe J et al [ 49 ] identified a crosstalk between Myc and activating transcription factor 2 (ATF2): Myc prolongs the half-life of ATF2 and causes increased phosphorylation of ATF2 at sites that have been shown to be crucial for the regulation of ATF2 activity [ 49 ]. Thus, ATF2 is activated by c-Myc on the protein level.…”

Section: Discussionmentioning

confidence: 99%

Transcription profiling of lung adenocarcinomas of c-myc-transgenic mice: Identification of the c-myc regulatory gene network

Reymann

Borlak

2008

BMC Syst Biol

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Background: The transcriptional regulator c-Myc is the most frequently deregulated oncogene in human tumors. Targeted overexpression of this gene in mice results in distinct types of lung adenocarcinomas. By using microarray technology, alterations in the expression of genes were captured based on a female transgenic mouse model in which, indeed, c-Myc overexpression in alveolar epithelium results in the development of bronchiolo-alveolar carcinoma (BAC) and papillary adenocarcinoma (PLAC). In this study, we analyzed exclusively the promoters of induced genes by different in silico methods in order to elucidate the c-Myc transcriptional regulatory network.

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Crosstalk between Myc and activating transcription factor 2 (ATF2): Myc prolongs the half-life and induces phosphorylation of ATF2

Cited by 7 publications

References 58 publications

ATF2 on the double – activating transcription factor and DNA damage response protein

ATF2 on the double – activating transcription factor and DNA damage response protein

Photodynamic Agents with Anti-metastatic Activities

Transcription profiling of lung adenocarcinomas of c-myc-transgenic mice: Identification of the c-myc regulatory gene network

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