ArticleThe Journal of biological chemistry2009
Redox mechanisms involved in the selective activation of Nrf2-mediated resistance versus p53-dependent apoptosis in adenocarcinoma cells.
Article in The Journal of biological chemistry, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 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
24 citing papers in PubMed, 45 citations in OpenAlex.
- Antioxidant Activity and Metabolomic Characterization ofMicroorganisms · 2026Article
- Indoxyl sulphate-initiated activation of cardiac fibroblasts is modulated by aryl hydrocarbon receptor and nuclear factor-erythroid-2-related factor 2.Journal of cellular and molecular medicine · 2024Article
- Bioactivity-guided fractionation ofFrontiers in cell and developmental biology · 2023Article
- Modulation of 1,2-Dicarbonyl Compounds in Postprandial Responses Mediated by Food Bioactive Components and Mediterranean Diet.Antioxidants (Basel, Switzerland) · 2022Review
- Review
- Article
- Non-esterified Fatty Acid Induce Dairy Cow Hepatocytes Apoptosis via the Mitochondria-Mediated ROS-JNK/ERK Signaling Pathway.Frontiers in cell and developmental biology · 2020Article
- Stress Marks on the Genome: Use or Lose?International journal of molecular sciences · 2019Review
- Antiproliferative activity of vitexin-2-O-xyloside and avenanthramides on CaCo-2 and HepG2 cancer cells occurs through apoptosis induction and reduction of pro-survival mechanisms.European journal of nutrition · 2018Article
- Cytoprotective Mechanisms Mediated by Polyphenols from Chilean Native Berries against Free Radical-Induced Damage on AGS Cells.Oxidative medicine and cellular longevity · 2017Article
- Mitochondrial permeabilization without caspase activation mediates the increase of basal apoptosis in cells lacking Nrf2.Free radical biology & medicine · 2016Article
- Functional Characterisation of Anticancer Activity in the Aqueous Extract of Helicteres angustifolia L. Roots.PloS one · 2016Article
- Article
- Cell survival following radiation exposure requires miR-525-3p mediated suppression of ARRB1 and TXN1.PloS one · 2013Article
- Subamolide a induces mitotic catastrophe accompanied by apoptosis in human lung cancer cells.Evidence-based complementary and alternative medicine : eCAM · 2013Article
- Expression of UDP-glucuronosyltransferase 1A, nuclear factor erythroid-E2-related factor 2 and Kelch-like ECH-associated protein 1 in colonic mucosa, adenoma and adenocarcinoma tissue.Oncology letters · 2012Article
- Glutathione and modulation of cell apoptosis.Biochimica et biophysica acta · 2012Review
- The effects of chromium(VI) on the thioredoxin system: implications for redox regulation.Free radical biology & medicine · 2012Review
- Article
- Chemistry of the cysteine sensors in Kelch-like ECH-associated protein 1.Antioxidants & redox signaling · 2010Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We have investigated the role of reactive oxygen species and thiol-oxidizing agents in the induction of cell death and have shown that adenocarcinoma gastric (AGS) cells respond differently to the oxidative challenge according to the signaling pathways activated. In particular, apoptosis in AGS cells is induced via the mitochondrial pathway upon treatment with thiol-oxidizing agents, such as diamide. Apoptosis is associated with persistent oxidative damage, as evidenced by the increase in carbonylated proteins and the expression/activation of DNA damage-sensitive proteins histone H2A.X and DNA-dependent protein kinase. Resistance to hydrogen peroxide is instead associated with Keap1 oxidation and rapid translocation of Nrf2 into the nucleus. Sensitivity to diamide and resistance to hydrogen peroxide are correlated with GSH redox changes, with diamide severely increasing GSSG, and hydrogen peroxide transiently inducing protein-GSH mixed disulfides. We show that p53 is activated in response to diamide treatment by the oxidative induction of the Trx1/p38(MAPK) signaling pathway. Similar results were obtained with another carcinoma cell line, CaCo2, indicating that these findings are not limited to AGS cells. Our data suggest that thiol-oxidizing agents could be exploited as inducers of apoptosis in tumor histotypes resistant to ROS-producing chemotherapeutics.
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.