ArticleOncogene2006
Altered regulation of c-jun and its involvement in anchorage-independent growth of human lung cancers.
Article in Oncogene, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
18 citing papers in PubMed, 37 citations in OpenAlex.
- Crosstalk between ROS-inflammatory gene expression axis in the progression of lung disorders.Naunyn-Schmiedeberg's archives of pharmacology · 2025Review
- Systematic analysis of apoptosis-related genes in the prognosis of lung squamous cell carcinoma: a combined single-cell RNA sequencing study.Journal of thoracic disease · 2023Article
- Induction of NUPR1 and AP‑1 contributes to the carcinogenic potential of nickel.Oncology reports · 2021Article
- A Comprehensive Network Pharmacology-Based Strategy to Investigate Multiple Mechanisms of HeChan Tablet on Lung Cancer.Evidence-based complementary and alternative medicine : eCAM · 2020Article
- APE1 modulates cellular responses to organophosphate pesticide-induced oxidative damage in non-small cell lung carcinoma A549 cells.Molecular and cellular biochemistry · 2018Article
- Gene Regulation Network Based Analysis Associated with TGF-βeta Stimulation in Lung Adenocarcinoma Cells.Iranian journal of biotechnology · 2017Article
- Retroviral cyclin controls cyclin-dependent kinase 8-mediated transcription elongation and reinitiation.Journal of virology · 2015Article
- Expression Of Selected Pathway-Marker Genes In Human Urothelial Cells Exposed Chronically To A Non-Cytotoxic Concentration Of Monomethylarsonous Acid.Toxicology reports · 2014Article
- Article
- Low level exposure to monomethyl arsonous acid-induced the over-production of inflammation-related cytokines and the activation of cell signals associated with tumor progression in a urothelial cell model.Toxicology and applied pharmacology · 2010Article
- SOX2 is an oncogene activated by recurrent 3q26.3 amplifications in human lung squamous cell carcinomas.PloS one · 2010Article
- c-Jun regulates phosphoinositide-dependent kinase 1 transcription: implication for Akt and protein kinase C activities and melanoma tumorigenesis.The Journal of biological chemistry · 2010Article
- Emerging roles of ATF2 and the dynamic AP1 network in cancer.Nature reviews. Cancer · 2010Review
- Simultaneous blockade of AP-1 and phosphatidylinositol 3-kinase pathway in non-small cell lung cancer cells.British journal of cancer · 2008Article
- Growth inhibition of non-small cell lung cancer cells by AP-1 blockade using a cJun dominant-negative mutant.British journal of cancer · 2008Article
- Apoptosis induction by antisense oligonucleotides against miR-17-5p and miR-20a in lung cancers overexpressing miR-17-92.Oncogene · 2007Article
- Aerosol-delivered programmed cell death 4 enhanced apoptosis, controlled cell cycle and suppressed AP-1 activity in the lungs of AP-1 luciferase reporter mice.Gene therapy · 2007Article
- Understanding signaling cascades in melanoma.Photochemistry and photobiologyReview
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The c-jun oncogene is frequently overexpressed in non-small-cell lung cancers (NSCLC), but its functional involvement in lung cancer development has not been clearly elucidated. In this study, we found that among the immediate-early serum responsible genes, exemplified by c-jun, c-fos and c-myc, induction of c-jun in a human bronchial epithelial cell line, BEAS-2B, was dependent on anchorage, in contrast to clear induction of c-fos and c-myc under both anchorage-dependent and -independent conditions. In fact, forced expression of c-jun in BEAS-2B cells significantly increased cell viability and colony formation in soft agar. Furthermore, we also found that such anchorage-dependent regulation of c-jun was lost in a significant fraction of human lung cancer cell lines. Interestingly, suppressed anchorage-independent but not anchorage-dependent growth was noted by constitutive expression of a dominant-negative c-jun mutant in a lung cancer cell line showing dysregulated and sustained c-jun expression in the absence of anchorage. These findings suggest that dysregulated c-jun expression may be involved in the acquisition of anchorage independence in the process of human lung carcinogenesis.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.