ArticleCell biochemistry and biophysics2026
Sanguinarine Antagonizes NSCLC Through PPARG-Mediated PI3K/AKT Suppression and Autophagic Apoptosis.
Article in Cell biochemistry and biophysics, 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.
- Lipid Modifications and Inflammation in Cardiometabolic and Vascular Disease: Perspectives from a Special Edition Honoring a Pioneer Scientist.Cell biochemistry and biophysics · 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
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Globally, non-small cell lung carcinoma (NSCLC) continues to be a major contributor to deaths from cancer. Sanguinarine (SNG), a naturally occurring benzophenanthridine alkaloid, has demonstrated considerable anti-cancer properties, yet its precise molecular mechanisms in NSCLC remain inadequately defined. Bioinformatic workflows comprised SNG target screening (TCMSP and SEA), acquisition of NSCLC-associated genes (GeneCards and CTD), PPI network assembly (STRING), and key target discovery through topological evaluation (Cytoscape). Gene Ontology/Kyoto Encyclopedia of Genes and Genomes enrichment analyses served to analyze target functional/pathway enrichment, while molecular docking validated SNG-core target binding. Experimentally, cell proliferation was assessed using Cell Counting Kit-8 and clonogenic assays. Apoptosis and autophagy were analyzed by flow cytometry, Western blot, and qRT-PCR. Computational pharmacology identified 16 principal molecular targets and emphasized the PI3K-AKT signaling pathway. SNG exhibited dose-responsive suppression of cellular viability and clonogenic capacity, alongside induction of apoptosis through BAX and BCL-2 regulation. Mechanistically, SNG triggered cytoprotective autophagy, evidenced by enhanced Beclin-1 expression, LC3-I to LC3-II conversion, and reduced p62 levels. Autophagy suppression markedly attenuated SNG’s anti-tumor activity. Moreover, SNG exhibited high binding affinity to key targets (ANXA5, STAT1, and Peroxisome Proliferator-Activated Receptor Gamma (PPARG)). Subsequent PPARG upregulation suppressed this critical oncogenic pathway. SNG exerts anti-neoplastic effects against NSCLC by promoting apoptosis and triggering cytoprotective autophagy, primarily through enhancing PPARG expression to suppress the PI3K-AKT signaling cascade.
Indexed as
Identifiers
41389163What Socratic 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 Socratic graph.