ArticleThe Journal of membrane biology2007
Both early and late stages of hepatocarcinogenesis are enhanced in Cx32 dominant negative mutant transgenic rats with disrupted gap junctional intercellular communication.
Article in The Journal of membrane biology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 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
10 citing papers in PubMed, 21 citations in OpenAlex.
- Lactoferrin Prevents Hepatic Injury and Fibrosis via the Inhibition of NF-κB Signaling in a Rat Non-Alcoholic Steatohepatitis Model.Nutrients · 2021Article
- Expression and Functionality of Connexin-Based Channels in Human Liver Cancer Cell Lines.International journal of molecular sciences · 2021Article
- A novel model of non-alcoholic steatohepatitis with fibrosis and carcinogenesis in connexin 32 dominant-negative transgenic rats.Archives of toxicology · 2020Article
- Cx32 exerts anti-apoptotic and pro-tumor effects via the epidermal growth factor receptor pathway in hepatocellular carcinoma.Journal of experimental & clinical cancer research : CR · 2019Article
- The role of gap junctions in inflammatory and neoplastic disorders (Review).International journal of molecular medicine · 2017Review
- Connexin-based signaling and drug-induced hepatotoxicity.Journal of clinical and translational research · 2017Article
- Transgenic rat models for mutagenesis and carcinogenesis.Genes and environment : the official journal of the Japanese Environmental Mutagen Society · 2017Review
- Connexin 32 dysfunction promotes ethanol-related hepatocarcinogenesis via activation of Dusp1-Erk axis.Oncotarget · 2016Article
- Localization of connexin 32 in spontaneous liver lesions of mice.The Journal of veterinary medical science · 2016Article
- Silencing of connexin 43 suppresses invasion, migration and lung metastasis of rat hepatocellular carcinoma cells.Cancer science · 2012Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Connexins are a family of transmembrane proteins essential for the gap junctions, which mediate cell-to-cell communication. Several connexins are reported to be tumor suppressors, and we have established transgenic (Tg) rats with a connexin 32 (Cx32) dominant negative mutant showing high sensitivity to early-stage diethylnitrosamine (DEN)-induced liver carcinogenesis. In this study, we carried out two independent experiments using Tg rats to further investigate the roles of disrupted Cx32 in late-stage carcinogenesis (carcinoma induction and metastasis) in the liver. In the first experiment, of 50 weeks' duration, DEN was administered at 6 weeks of age and at 26 weeks to explore the effects of carcinogen treatments at different stages. The number of hepatocellular carcinomas (HCCs) was significantly increased in Tg compared with non-Tg rats. The second experiment focused on the effects of Cx32 disruption on metastasis by HCCs induced by administration of DEN and N-nitrosomorpholine. Only Tg rats had multiple metastases of HCCs in the lung, and the development and growth of HCCs was dramatically accelerated in Tg compared to non-Tg rats. Thus, normal function of Cx32 may be essential for suppression of both early and late stages of hepatocarcinogenesis.
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.