ArticleBritish journal of cancer2008
Simultaneous blockade of AP-1 and phosphatidylinositol 3-kinase pathway in non-small cell lung cancer cells.
Article in British journal of cancer, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 18 citations in OpenAlex.
- The human adenovirus E1B-55K oncoprotein coordinates cell transformation through regulation of DNA-bound host transcription factors.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
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- MiR-1299 Impedes the Progression of Non-Small-Cell Lung Cancer Through EGFR/PI3K/AKT Signaling Pathway.OncoTargets and therapy · 2020Article
- Study on the Mechanism of Ginseng in the Treatment of Lung Adenocarcinoma Based on Network Pharmacology.Evidence-based complementary and alternative medicine : eCAM · 2020Article
- Chrysotile effects on the expression of anti-oncogene P53 and P16 and oncogene C-jun and C-fos in Wistar rats' lung tissues.Environmental science and pollution research international · 2018Article
- Novel link between prostaglandin E2 (PGE2) and cholinergic signaling in lung cancer: The role of c-Jun in PGE2-induced α7 nicotinic acetylcholine receptor expression and tumor cell proliferation.Thoracic cancer · 2015Article
- Article
- Dependence on the MUC1-C oncoprotein in non-small cell lung cancer cells.Molecular cancer therapeutics · 2011Article
- Claudins 10 and 18 are predominantly expressed in lung adenocarcinomas and in tumors of nonsmokers.International journal of clinical and experimental pathology · 2011Article
- A dominant-negative c-jun mutant inhibits lung carcinogenesis in mice.Cancer prevention research (Philadelphia, Pa.) · 2010Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
Abstract
c-Jun is a major constituent of AP-1 transcription factor that transduces multiple mitogen growth signals, and it is frequently overexpressed in non-small cell lung cancers (NSCLCs). Earlier, we showed that blocking AP-1 by the overexpression of a c-Jun dominant-negative mutant, TAM67, inhibited NSCLC cell growth. The phosphatidylinositol 3-kinase (PI3K)/Akt signal transduction pathway is important in transformation, proliferation, survival and metastasis of NSCLC cells. In this study, we used NCI-H1299 Tet-on clone cells that express TAM67 under the control of inducible promoter to determine the effects of inhibition of AP-1 and PI3K on cell growth. The PI3K inhibitor, LY294002, produced a dose-dependent inhibition of growth in H1299 cells and that inhibition was enhanced by TAM67. TAM67 increased dephosphorylation of Akt induced by LY294002 and reduced the TPA response element DNA-binding of phosphorylated c-Jun. TAM67 increased G1 cell cycle blockade induced by LY294002, which was partially associated with cyclin A decrease and p27(Kip1) accumulation. Furthermore, TAM67 and LY294002 act, at least additively, to inhibit anchorage-independent growth of the H1299 cells. These results suggest that AP-1 and PI3K/Akt pathways play an essential role in the growth of some NSCLC cells.
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