ReviewCancer cell international2026
C-MYC as a key effector of WNT, PI3K/AKT, MAPK, and TGF-β signaling pathways in regulation of epithelial-mesenchymal transition during tumor metastasis.
Review in Cancer cell international, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed.
- Berberine inhibits gastric cancer progression by targeting canonical Wnt/β-catenin signaling in AGS cells.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Epithelial-mesenchymal transition (EMT) is a key cellular process that facilitates distant metastasis during tumor progression. Tumor cells lose their epithelial characteristics while obtaining mesenchymal features during EMT process. This process is associated with a complex interaction between tumor cells, microenvironment, and signaling pathways. Therefore, it is helpful to clarify the molecular mechanisms of EMT process to introduce novel diagnostic and therapeutic markers to target malignant tumor cells. C-MYC is a transcription factor that regulates cell proliferation, apoptosis, metabolism, and EMT process. C-MYC is an effector of various signaling pathways that regulates EMT process during tumor progression. Therefore, in the present review we discussed the role of signaling pathways in regulation of C-MYC mediated EMT process during tumor progression. It has been shown that WNT, MAPK, TGF-β, and PI3K/AKT pathways are the main regulators of C-MYC mediated EMT process in tumor cells. This review paves the way to introduce C-MYC as a reliable therapeutic target to reduce metastatic ability of tumor cells.
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.