ArticleOncogene2008
TCDD deregulates contact inhibition in rat liver oval cells via Ah receptor, JunD and cyclin A.
Article in Oncogene, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 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
27 citing papers in PubMed, 77 citations in OpenAlex.
- Cell-cell contacts prevent t-BuOOH-triggered ferroptosis and cellular damage in vitro by regulation of intracellular calcium.Archives of toxicology · 2024Article
- The evolution and structure/function of bHLH-PAS transcription factor family.Biochemical Society transactions · 2022Review
- Ferroptosis Meets Cell-Cell Contacts.Cells · 2021Review
- Mechanisms of circadian clock interactions with aryl hydrocarbon receptor signalling.The European journal of neuroscience · 2020Article
- Rapid Analysis of Effects of Environmental Toxicants on Tumorigenesis and Inflammation Using a Transgenic Zebrafish Model for Liver Cancer.Marine biotechnology (New York, N.Y.) · 2019Article
- AhR signaling pathways and regulatory functions.Biochimie open · 2018Review
- Xenobiotica-metabolizing enzymes in the skin of rat, mouse, pig, guinea pig, man, and in human skin models.Archives of toxicology · 2018Review
- Pure non-dioxin-like PCB congeners suppress induction of AhR-dependent endpoints in rat liver cells.Environmental science and pollution research international · 2016Article
- Environmental Ligands of the Aryl Hydrocarbon Receptor and Their Effects in Models of Adult Liver Progenitor Cells.Stem cells international · 2016Review
- Antioxidant Functions of the Aryl Hydrocarbon Receptor.Stem cells international · 2016Review
- New Trends in Aryl Hydrocarbon Receptor Biology.Frontiers in cell and developmental biology · 2016Review
- Anticancer activity of 7-epiclusianone, a benzophenone from Garcinia brasiliensis, in glioblastoma.BMC complementary and alternative medicine · 2015Article
- Assessing the carcinogenic potential of low-dose exposures to chemical mixtures in the environment: focus on the cancer hallmark of tumor angiogenesis.Carcinogenesis · 2015Review
- Mechanisms of environmental chemicals that enable the cancer hallmark of evasion of growth suppression.Carcinogenesis · 2015Review
- Lineage-dependent effects of aryl hydrocarbon receptor agonists contribute to liver tumorigenesis.Hepatology (Baltimore, Md.) · 2015Article
- Recent advances in 2D and 3D in vitro systems using primary hepatocytes, alternative hepatocyte sources and non-parenchymal liver cells and their use in investigating mechanisms of hepatotoxicity, cell signaling and ADME.Archives of toxicology · 2013Review
- Aryl hydrocarbon receptor activation attenuates Per1 gene induction and influences circadian clock resetting.Toxicological sciences : an official journal of the Society of Toxicology · 2013Article
- Modeling drug- and chemical-induced hepatotoxicity with systems biology approaches.Frontiers in physiology · 2012Article
- Ah receptor antagonism inhibits constitutive and cytokine inducible IL6 production in head and neck tumor cell lines.Molecular carcinogenesis · 2011Article
- Aryl hydrocarbon receptor nuclear translocator in hepatocytes is required for aryl hydrocarbon receptor-mediated adaptive and toxic responses in liver.Toxicological sciences : an official journal of the Society of Toxicology · 2010Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The aryl hydrocarbon receptor (AhR) is a transcription factor involved in physiological processes, but also mediates most, if not all, toxic responses to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). Activation of the AhR by TCDD leads to its dimerization with aryl hydrocarbon nuclear translocator (ARNT) and transcriptional activation of several phase I and II metabolizing enzymes. However, this classical signalling pathway so far failed to explain the pleiotropic hazardous effects of TCDD, such as developmental toxicity and tumour promotion. Thus, there is an urgent need to define genetic programmes orchestrated by AhR to unravel its role in physiology and toxicology. Here we show that TCDD treatment of rat liver oval cells leads to induction of the transcription factor JunD, resulting in transcriptional upregulation of the proto-oncogene cyclin A which finally triggers a release from contact inhibition. Ectopic expression of cyclin A in confluent cultures overcomes G(1) arrest, indicating that increased cyclin A levels are indeed sufficient to bypass contact inhibition. Functional interference with AhR-, but not with ARNT, abolished TCDD-induced increase in JunD and cyclin A and prevented loss of contact inhibition. In summary, we have discovered a novel AhR-dependent and probably ARNT-independent signalling pathway involving JunD and cyclin A, which mediates TCDD-induced deregulation of cell cycle control.
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.