ArticleOncogene2005
Deficiency in the gap junction protein connexin32 alters p27Kip1 tumor suppression and MAPK activation in a tissue-specific manner.
Article in Oncogene, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 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
29 citing papers in PubMed, 50 citations in OpenAlex.
- Preclinical In Vitro Model to Assess the Changes in Permeability and Cytotoxicity of Polarized Intestinal Epithelial Cells during Exposure Mimicking Oral or Intravenous Routes: An Example of Arsenite Exposure.International journal of molecular sciences · 2022Article
- Article
- Progress in the application of organoids to breast cancer research.Journal of cellular and molecular medicine · 2020Review
- Connexins in Lung Cancer and Brain Metastasis.Frontiers in oncology · 2020Review
- Article
- Article
- Noise-resistant developmental reproducibility in vertebrate somite formation.PLoS computational biology · 2019Article
- Therapeutic strategies targeting connexins.Nature reviews. Drug discovery · 2018Review
- Cell-Cell Junctions Organize Structural and Signaling Networks.Cold Spring Harbor perspectives in biology · 2018Review
- Connexin-based signaling and drug-induced hepatotoxicity.Journal of clinical and translational research · 2017Article
- Gap junctions and cancer: communicating for 50 years.Nature reviews. Cancer · 2016Review
- Connexin 32 dysfunction promotes ethanol-related hepatocarcinogenesis via activation of Dusp1-Erk axis.Oncotarget · 2016Article
- Connexin and pannexin signaling in gastrointestinal and liver disease.Translational research : the journal of laboratory and clinical medicine · 2015Review
- The lung communication network.Cellular and molecular life sciences : CMLS · 2015Review
- Connexin 30 expression inhibits growth of human malignant gliomas but protects them against radiation therapy.Neuro-oncology · 2015Article
- GATA-3 augmentation down-regulates Connexin43 in Helicobacter pylori associated gastric carcinogenesis.Cancer biology & therapy · 2015Article
- MicroRNA signature characterizes primary tumors that metastasize in an esophageal adenocarcinoma rat model.PloS one · 2015Article
- Vitamin D3 regulates the formation and degradation of gap junctions in androgen-responsive human prostate cancer cells.PloS one · 2014Article
- Gap junctions.Comprehensive Physiology · 2012Review
- Evaluating the role of connexin43 in congenital heart disease: Screening for mutations in patients with outflow tract anomalies and the analysis of knock-in mouse models.Journal of cardiovascular disease research · 2011Article
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 2 institutions in 2 countries.
Funding
Abstract
Connexin32 knockout mice (Cx32-KO) exhibit increased chemical- and radiation-induced liver and lung tumor formation with many lung tumors demonstrating decreased levels of the tumor suppressor p27KIP1. To determine if p27 deficiency alters Cx32-influenced tumorigenesis, we have generated a Cx32/p27 double-deficient mouse strain (DKO) and show here that exposure of these mice to X-ray radiation resulted in an increase or decrease in tumorigenesis depending on the tissue. Several tissues were highly sensitive to loss of p27 tumor suppressor function (intestine, adrenal, pituitary) resulting in an increased overall tumor burden in DKO mice compared to both wild-type (P<0.005) and Cx32-KO mice (P=0.066). However, additional deletion of p27 in a Cx32-KO background resulted in a statistically significant decrease in the liver tumor incidence suggesting that Cx32 and p27 pathways mechanistically interact. Immunohistochemical analysis revealed an increased percentage of Cx32-KO liver and lung tumors harboring active mitogen-activated protein kinase (Erk1, Erk2) pathways in contrast to lower percentages of activated wild-type (P<0.005) and DKO tumors (P=0.027). Increased MAPK activation in liver tumors did not correlate with Ha-ras codon-61 mutation status. This study demonstrates that tissues dependent on Cx32 tumor suppression, such as the liver and lung, exhibit altered tumorigenesis and tumor biology (MAPK pathway activation) related to p27 status.
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.