ArticleOncology letters2026
D-salicin induces oxidative stress-mediated ERK1/2 suppression and apoptosis in endometrial cancer cells.
Article in Oncology letters, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Endometrial cancer is a common gynecologic malignancy for which therapeutic options remain limited in advanced or treatment-resistant disease. Natural compounds that selectively perturb cancer-associated redox signaling and survival pathways may offer novel anticancer strategies. The present study investigated the anticancer effects of D-salicin in the endometrial adenocarcinoma-derived Ishikawa cell line, with a focus on oxidative stress and extracellular signal-regulated kinase (ERK)1/2 signaling, and assessed cancer selectivity using normal human dermal fibroblasts (HDF). D-salicin selectively reduced Ishikawa cell viability in a concentration-dependent manner while largely sparing HDF. This cytotoxic effect was accompanied by marked intracellular reactive oxygen species (ROS) accumulation, increased lipid peroxidation (MDA) and depletion of total glutathione (GSH), indicating induction of oxidative stress. Elevated oxidative burden was associated with caspase-3 activation and concentration-dependent suppression of ERK1/2 phosphorylation, both of which were attenuated by N-acetylcysteine (NAC) co-treatment. To determine redox dependence, NAC was incorporated as an antioxidant co-treatment. D-salicin induced a significant, concentration-dependent reduction in Ishikawa cell viability (P
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.