ArticleThe Journal of biological chemistry2011
Auto-activation of c-JUN gene by amino acid deprivation of hepatocellular carcinoma cells reveals a novel c-JUN-mediated signaling pathway.
Article in The Journal of biological chemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 37 citations in OpenAlex.
- An RNA-sequencing analysis to determine potential upstream transcriptional regulators of essential amino acid deficiency responses in bovine mammary epithelial cells.BMC genomics · 2026Article
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- Effects of lysine and methionine on mRNA expression of candidate transcription factors by primary bovine mammary epithelial cells.PloS one · 2024Article
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- Regulation of Hepatic Metabolism and Cell Growth by the ATF/CREB Family of Transcription Factors.Diabetes · 2021Review
- Oncogenic K-Ras4B Dimerization Enhances Downstream Mitogen-activated Protein Kinase Signaling.Journal of molecular biology · 2020Article
- Induction of early growth response gene 1 (EGR1) by endoplasmic reticulum stress is mediated by the extracellular regulated kinase (ERK) arm of the MAPK pathways.Biochimica et biophysica acta. Molecular cell research · 2019Article
- A circRNA-miRNA-mRNA network identification for exploring underlying pathogenesis and therapy strategy of hepatocellular carcinoma.Journal of translational medicine · 2018Article
- Promotional effect of microRNA-194 on breast cancer cells via targeting F-box/WD repeat-containing protein 7.Oncology letters · 2018Article
- Regulation of the ATF3 gene by a single promoter in response to amino acid availability and endoplasmic reticulum stress in human primary hepatocytes and hepatoma cells.Biochimica et biophysica acta. Gene regulatory mechanisms · 2018Article
- MAPK signaling triggers transcriptional induction of cFOS during amino acid limitation of HepG2 cells.Biochimica et biophysica acta · 2015Article
- A mitogen-activated protein kinase/extracellular signal-regulated kinase kinase (MEK)-dependent transcriptional program controls activation of the early growth response 1 (EGR1) gene during amino acid limitation.The Journal of biological chemistry · 2014Article
- Galectin-1 overexpression promotes progression and chemoresistance to cisplatin in epithelial ovarian cancer.Cell death & disease · 2014Article
- ATF2 knockdown reinforces oxidative stress-induced apoptosis in TE7 cancer cells.Journal of cellular and molecular medicine · 2013Article
- Activation of the amino acid response modulates lineage specification during differentiation of murine embryonic stem cells.American journal of physiology. Endocrinology and metabolism · 2013Article
- Asparagine synthetase: regulation by cell stress and involvement in tumor biology.American journal of physiology. Endocrinology and metabolism · 2013Review
- Elevated cJUN expression and an ATF/CRE site within the ATF3 promoter contribute to activation of ATF3 transcription by the amino acid response.Physiological genomics · 2013Article
- Acidosis blocks CCAAT/enhancer-binding protein homologous protein (CHOP)- and c-Jun-mediated induction of p53-upregulated mediator of apoptosis (PUMA) during amino acid starvation.Biochemical and biophysical research communications · 2013Article
- Dynamic changes in genomic histone association and modification during activation of the ASNS and ATF3 genes by amino acid limitation.The Biochemical journal · 2013Article
- A coregulatory network of NR2F1 and microRNA-140.PloS one · 2013Article
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Mammalian cells respond to protein or amino acid (AA) limitation by activating a number of signaling pathways, collectively referred to as the AA response (AAR), that modulate a range of cellular functions, including transcriptional induction of target genes. This study demonstrates that in hepatocellular carcinoma cells, expression of c-JUN, JUN-B, c-FOS, and FOS-B was induced by the AAR, whereas JUN-D, FRA-1, and FRA-2 were not. Of the four activated FOS/JUN members, c-JUN made the largest contribution to the induction of several known AAR target genes. For several human liver, prostate, and ovarian cell lines, the AAR-induced increase in c-JUN expression was greater in transformed cells compared with nontransformed counterparts, an effect independent of cell growth rate. Thus far, the best characterized AA-responsive genes are all transcriptionally activated by ATF4, but the AAR-dependent induction of c-JUN transcription was ATF4-independent. The increased expression of c-JUN was dependent on ATF2 and on activation of the MEK-ERK and JNK arms of the MAPK signaling pathways. Formation of c-JUN-ATF2-activated heterodimers was increased after AA limitation, and c-JUN or ATF2 knockdown suppressed the induction of c-JUN and other AAR target genes. AA deprivation triggers a feed-forward process that involves phosphorylation of existing c-JUN protein by JNK and subsequent auto-activation of the c-JUN gene by recruitment of c-JUN and ATF2 to two AP-1 sites within the proximal promoter. The results document the novel observation that AP-1 sequences within the c-JUN gene can function as transcriptional amino acid-response elements.
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