ArticleCancer science2026
Adipocyte-Derived Palmitic Acid Promotes Breast Cancer Malignancy via ZDHHC15-Mediated S-Palmitoylation of PPARγ.
Article in Cancer science, 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.
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
Peroxisome proliferator-activated receptor gamma (PPARγ), a well-characterized regulator of adipogenesis, also functions as a tumor suppressor in breast cancer. However, the PPARγ agonist rosiglitazone has shown limited clinical efficacy, highlighting the importance of understanding PPARγ regulation within the tumor microenvironment. Here, we demonstrate that adipocyte-derived palmitic acid promotes PPARγ S-palmitoylation via zinc finger DHHC-domain containing protein 15 (ZDHHC15), as confirmed by acyl-biotin exchange (ABE) assay. Immunoblot, RT-qPCR, and immunoprecipitation further revealed that this modification leads to ubiquitin-mediated proteasomal degradation of PPARγ. Functional studies using adipocyte-conditioned media and an oxygen-permeable 3D spheroid culture system showed that PPARγ palmitoylation promotes breast cancer malignancy and confers resistance to rosiglitazone. Notably, the palmitoylation inhibitor 2-bromopalmitate (2-BP) stabilizes PPARγ, suppressing breast cancer malignancy. Furthermore, 2-BP synergistically enhances the therapeutic efficacy of rosiglitazone, suggesting that targeting PPARγ S-palmitoylation represents a promising therapeutic strategy in breast cancer.
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.