ArticleMolecular and cellular biochemistry2026
Targeting the Wnt/β-catenin pathway: veratramine mitigates MNNG-induced gastric precancerous lesions.
Article in Molecular and cellular biochemistry, 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
10 authors.
Funding
Abstract
Gastric precancerous lesions (GPLs) are a pivotal stage in the gastritis-gastric cancer sequence, and the absence of effective treatments presents a clinical challenge. Veratramine is a natural anti-inflammatory and analgesic steroid alkaloid; however, its effects on GPLs and the mechanisms have remained unexplored. This study investigated the effects of veratramine on GPLs using 1-Methyl-3-nitro-1-nitrosoguanidine (MNNG)-induced GES-1 cells and rat models, utilizing RNA-seq to elucidate the underlying mechanisms. In vitro, veratramine inhibited malignant cells (MC) proliferation, induced apoptosis, and triggered G0/G1 cell cycle arrest. It also suppressed epithelial-mesenchymal transition (EMT), migration, and invasion by upregulating E‑cadherin and downregulating Slug and vimentin. Transcriptomic and molecular docking analyses highlighted the Wnt/β-catenin pathway as a key target, regulated via DDX60, MUC1, APOL1, and MSH5. Veratramine reduced Wnt10B, β-catenin, and cyclin D1 expression and blocked β‑catenin nuclear translocation; these effects were reversed by the Wnt activator BML-284. In vivo, treatment with veratramine ameliorated the GPLs-induced pathological changes in rats. It restored body weight and preserved gastric mucosal integrity, as evidenced by intact glandular and cellular morphology, reduced hyperplasia, and attenuated intestinal metaplasia. These improvements were associated with a modulation of key molecular markers, specifically a decrease in the expression of N-cadherin, Wnt10B, and β-catenin, alongside an increase in E-cadherin expression in gastric tissues. These results collectively indicate that veratramine exerts its therapeutic effects against GPLs primarily by suppressing the Wnt/β-catenin signaling pathway. Taken together, our findings suggest that veratramine is a promising candidate small-molecule drug for the treatment of GPLs.
Indexed as
Identifiers
42530764What 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.