Activation of Nonsteroidal Anti-Inflammatory Drug-Activated Gene-1 via Extracellular Signal-Regulated Kinase 1/2 Mitogen-Activated Protein Kinase Revealed a Isochaihulactone-Triggered Apoptotic Pathway in Human Lung Cancer A549 Cells
The Journal of Pharmacology and Experimental Therapeutics, ISSN: 0022-3565, Vol: 323, Issue: 2, Page: 746-756
2007
- 42Citations
- 19Captures
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Metrics Details
- Citations42
- Citation Indexes42
- CrossRef42
- 41
- Captures19
- Readers19
- 19
Article Description
The novel lignan isochaihulactone inhibits cell proliferation and is an effective inducer of apoptosis in a variety of carcinoma cell lines. To determine the mechanisms underlying these effects, we examined isochaihulactone-induced changes in gene expression using oligodeoxynucleotide-based microarray screening of a human lung carcinoma cell line, A549. Isochaihulactone-inducible genes included the early growth response gene-1 ( EGR-1 ) and nonsteroidal anti-inflammatory drug-activated gene ( NAG-1 ). Isochaihulactone increased EGR-1 and then NAG-1 mRNA and protein expression. Pure isochaihulactone induced phosphorylation of extracellular signal-regulated kinase (ERK) 1/2. Isochaihulactone-induced increases in EGR-1 and NAG-1 expression were reduced by the mitogen-activated protein kinase kinase 1/2 inhibitor 2′-amino-3′-methoxyflavone (PD98059), and this effect was not blocked by the phosphatidylinositol 3-kinase/protein kinase B pathway inhibitor 2-(4-morpholinyl)-8-phenyl-1(4 H )-benzopyran-4-one hydrochloride (LY294002). Inhibition of isochaihulactone-induced NAG-1 expression by EGR-1 small interfering RNA blocked isochaihulactone-induced apoptosis in A549 cells, suggesting that induction of EGR-1 expression decreases survival of A549 cells. RNA interference using double-stranded RNA specific for NAG-1 also inhibited isochaihulactone-induced apoptosis, and cells transfected to increased NAG-1 expression had a greater apoptotic response to isochaihulactone and reduced colony formation efficiency. In addition, treatment of nude mice with isochaihulactone increased the in vivo NAG-1 expression as examined by immunohistochemistry from tumor biopsy. Isochaihulactone treatment increased the luciferase activity of NAG-1 in A549 cells transfected with the NAG-1 promoter construct. This induction increased expression of NAG-1 that was p53-independent and Sp1-dependent. Our findings suggest that NAG-1 expression is up-regulated by isochaihulactone through an ERK-dependent pathway involving the activation of EGR-1.
Bibliographic Details
http://www.sciencedirect.com/science/article/pii/S0022356524341631; http://dx.doi.org/10.1124/jpet.107.126193; http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=35548995873&origin=inward; http://www.ncbi.nlm.nih.gov/pubmed/17715378; https://linkinghub.elsevier.com/retrieve/pii/S0022356524341631; https://dx.doi.org/10.1124/jpet.107.126193; https://jpet.aspetjournals.org/content/323/2/746
Elsevier BV
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