Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
<b>Rationale</b>: Activating transcription factor 4 (ATF4) is a central regulator of the cellular stress response and reduces tumor burden by controlling the expression of target genes implicated in the induction of apoptosis.
|
31534554 |
2019 |
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
We found that the ATF4/p-eIF2α pathway is activated in response to Sunitinib in primary tumor initiating progenitor cell cultures (BTICs).
|
30719230 |
2019 |
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Furthermore, we identified ATF4 target genes (<i>LZTFL1, MKNK2</i>, and <i>SIAH1</i> with known tumor suppressor function) that were synergistically upregulated with the combination of TKI and ERAD inhibitor.
|
30552230 |
2019 |
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
In addition, endoplasmic reticulum (ER) stress in tumor samples or cells was markedly induced by CA treatment through promoting the expression of associated signals such as Parkin, protein kinase RNA-like ER kinase (PERK), activating transcription factors 4 (ATF4) and ATF6.
|
31545234 |
2019 |
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Relationship between TGFβ and ATF4, their effects on aggressiveness (tumor proliferation, metastasis, and stemness), and the underlying pathways were analyzed in three TNBC cell lines and <i>in vivo</i> using patient-derived xenografts (PDX).<b>Results:</b><i>ATF4</i> overexpression correlated with TNBC patient survival decrease and a SMAD-dependent crosstalk between ATF4 and TGFβ was identified.
|
30012564 |
2018 |
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Finally, indicators of UPR, PERK, p-eIF2α and GRP78, increased (<i>p</i> < 0.05), whereas ATF4 was strongly decreased (<i>p</i> < 0.01) in the liver of tumor-bearing mice while sACVR2B-Fc had no effect.
|
30713500 |
2018 |
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
The eIF2<i>α</i>/ATF4 pathway is responsible for the integrated stress response (ISR) of unfolded protein response (UPR) which can affect immune cell function in tumor microenvironment.
|
30305853 |
2018 |
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
We found decreased or loss of ATF4 in 52% of MTC tumors (n = 39) compared with normal thyroid follicle cells.
|
27935748 |
2017 |
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
ATF4, a key transcription mediator of the integrated stress response, also activates AXL and suppresses senescence to impose the MITF-low/AXL-high drug-resistant phenotype observed in human tumors.
|
28096186 |
2017 |
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Taken together, our findings suggest that ATF4 contributes to tumor growth of EC by promoting CCL2 and subsequent recruitment of macrophage, and that ATF4/CCL2 axis might be a potential therapeutic target for EC.
|
28843961 |
2017 |
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Further experiments revealed that ATF4-dependent tumor promoting effects are mediated by transcriptional targeting the glutamate antiporter xCT/SCL7A11 (also known as system Xc<sup>-</sup>).
|
28553953 |
2017 |
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Our data show that ATF4 operates as a chemo-resistance gene in gliomas, and the tumor promoting function of ATF4 is mainly determined by its transcriptional target xCT.
|
28881638 |
2017 |
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
ATF4 upregulation by p62 deficiency in the stroma activates glucose carbon flux through a pyruvate carboxylase-asparagine synthase cascade that results in asparagine generation as a source of nitrogen for stroma and tumor epithelial proliferation.
|
28988820 |
2017 |
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Mice injected with ATF4-overexpressing cells exhibited a higher rate of tumor growth, and the average weight of these tumors was ~90% greater than the controls.
|
26797758 |
2016 |
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Nutritional Stress Induced by Tryptophan-Degrading Enzymes Results in ATF4-Dependent Reprogramming of the Amino Acid Transporter Profile in Tumor Cells.
|
27651314 |
2016 |
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
ATF4-deficient human fibrosarcoma cells were unable to colonize the lungs in a murine model, and reconstitution of ATF4 or HO-1 expression in ATF4-deficient cells blocked anoikis and rescued tumor lung colonization.
|
26011642 |
2015 |
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Impairment of hypoxia-inducible factor 1α, endoplasmic reticulum stress (IRE1α/XBP1), and the crosstalk between activating transcription factor 3/activating transcription factor 4 and transforming growth factor β was observed. iNOS inhibition significantly reduced tumor growth, the number of lung metastases, tumor initiation, and self-renewal.
|
25849745 |
2015 |
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
These results suggest that AA induces tumor cell apoptosis associated with ATF4-dependent ER stress.
|
24853302 |
2014 |
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Our results reveal that the GCN2/ATF4 pathway promotes tumor growth and angiogenesis through AAD-mediated VEGF expression and, thus, is a potential target in cancer therapy.
|
23908598 |
2013 |
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Consequently, either ATF4 agonists or glutaminolysis inhibitors potently induce apoptosis in vitro and inhibit tumor growth in vivo.
|
23153536 |
2012 |
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
It has been reported that activating transcription factor 4 (ATF4) increases the processes of tumor growth, metastasis and drug resistance.
|
22338651 |
2012 |
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Furthermore, these data suggest that ATF4 status may be a critical determinant of the ability of cancer cells to adapt to oxygen and acidity fluctuations in the tumor microenvironment, perhaps linking short-term transcriptional responses to long-term selection for copy number alterations in cancer cells.
|
22135092 |
2012 |
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
Here we summarize recent findings regarding the regulation of ATF4 in transformed cells, clinical tumor samples and tumor models, and speculate on its potential role in tumor progression and chemoresistance.
|
19519398 |
2009 |
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Since ATF4 is induced by tumour microenvironmental factors, and regulates processes relevant to cancer progression, it might serve as a potential therapeutic target in cancer.
|
17466566 |
2008 |
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
Activating transcription factor 4 (ATF4) is a mediator of the UPR and activates a gene expression program, promoting tumour growth and survival under anoxia.
|
18408768 |
2008 |