ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2026
CEBPG-Mediated Palmitic Acid Adaptation of Cancer-Associated Fibroblasts Drives Metastasis of Oral Squamous Cell Carcinoma.
Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 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
7 authors.
Funding
Abstract
Fatty acids (FAs) create a pro-metastatic niche in multiple cancers, but how the tumor microenvironment (TME) counteracts FA stress remains unclear. Here, we found that the FA transporter CD36 was upregulated in myofibroblastic cancer-associated fibroblasts (myoCAFs), where it correlated with the metastasis of oral squamous cell carcinoma (OSCC). Among five predominant FA species enriched in OSCC tissues, palmitic acid (PA) potently activated myoCAF phenotypes across 2D, 3D, and organoid co-culture models. In vivo, PA promoted lymph node metastasis in orthotopic tumors comprising OSCC cells and CAFs, an effect abolished by CD36 knockdown in cancer-associated fibroblasts (CAFs). Mechanistically, PA remodeled the chromatin landscape to enhance H3K27ac occupancy at multiple genes including ERN1 and TMBIM6, two stress-adaptive regulators. Transcription of ERN1 and TMBIM6 in CAFs was regulated by CCAAT/enhancer-binding protein γ (CEBPG) in an enhancer-associated manner. Disruption of the CEBPG-IRE1α/TMBIM6 axis attenuated myoCAFs properties and abrogated PA-driven metastasis. Our results unveil a stromal metabolic checkpoint and establish CEBPG-mediated stress resilience as a therapeutic target to curtail metastasis. Significance: Palmitic acid promotes metastasis via a stromal CEBPG-IRE1α/TMBIM6 axis, uncovering a metabolic vulnerability that offers novel therapeutic targets to inhibit oral squamous cell carcinoma.
Indexed as
Identifiers
What 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.