ArticleJournal of experimental & clinical cancer research : CR2019
CD36 mediates palmitate acid-induced metastasis of gastric cancer via AKT/GSK-3β/β-catenin pathway.
Article in Journal of experimental & clinical cancer research : CR, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 156 papers.
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Who cites it
156 citing papers in PubMed, 221 citations in OpenAlex.
- Fatty acid 2-hydroxylation restrains gastric cancer by blocking CD36 palmitoylation and fatty acid uptake.Oncogene · 2026Article
- Targeting JOSD2 degrades β-catenin to suppress colorectal cancer metastasis by disrupting RAS/ERK/β-catenin axis.Acta pharmacologica Sinica · 2026Article
- THBS2: the key hub linking breast cancer stroma, immunity, and therapeutic response.Clinical & experimental metastasis · 2026Review
- Palmitate promotes liver metastases by decreasing neutrophil antitumour behaviour.Nature metabolism · 2026Article
- Fatty acid metabolic reprogramming in the tumor microenvironment: Unraveling mechanisms and therapeutic prospects.Genes & diseases · 2026Review
- Prognostic biomarkers for lung adenocarcinoma based on Mendelian randomization analysis.The Journal of international medical research · 2026Article
- L-type calcium channel-mediated lipid metabolic reprogramming in gastric adenocarcinoma progression.Translational oncology · 2026Article
- Optimizing Component Formula Extracted from Ginseng and Salvia Inhibits Lung Cancer Metastasis and EMT via Suppressing AKT/GSK-3β/β-catenin Pathway.Journal of ginseng research · 2026Article
- The VAX2-SERPINE1 axis modulates colorectal cancer cell proliferation and apoptosis through WNT/beta-catenin signaling.Translational oncology · 2026Article
- PCDHGC3 silencing promotes clear cell renal cell carcinoma metastasis via mTOR/HIF2α activation, lipid metabolism rewiring, and ferroptosis evasion.Cell death & disease · 2026Article
- Solute Carrier transporters in tumor metabolism and immune modulation: implications for therapy.Journal of translational medicine · 2026Review
- Targeting fatty acid metabolism for cancer therapy.Fundamental research · 2026Review
- Nobiletin and polydatin synergistically alleviate triple-negative breast cancer liver metastasis via suppressing ECM1a-mediated fatty acid biosynthesis.Acta pharmacologica Sinica · 2026Article
- Metabolic crosstalk among cancer-associated fibroblasts, adipocytes and immune cells as an immunosuppressive tumor microenvironment driver.Experimental & molecular medicine · 2026Review
- Tumor microenvironment dynamics in gastric cancer pathogenesis and therapeutic resistance.Molecular cancer · 2026Review
- Mechanisms of Metabolic Reprogramming Regulating Immunosuppression in the Gastric Cancer Tumor Microenvironment.Biomolecules · 2026Review
- Targeting the remodeled peritoneal ecosystem: a paradigm shift from tumor cells to the microenvironment in gastric cancer peritoneal metastasis.Frontiers in immunology · 2026Review
- Metabolic adaptations in cancer progression.Physiological reviews · 2026Review
- Banxia xiexin decoction and its bioactive metabolites: multi-targeted mechanisms for suppressing gastric cancer progression, reversing chemoresistance, and remodeling the tumor microenvironment.Frontiers in pharmacology · 2026Review
- Lipid metabolism and the immune microenvironment in gastric cancer.Frontiers in immunology · 2026Review
96 more citing papers are in PubMed but not listed here.
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundGastric cancer (GC) has a clear predilection for metastasis toward the omentum which is primarily composed of adipose tissue, indicating that fatty acids may contribute to this phenomenon. However their function remains poorly understood in GC. In this study, we investigated the role of palmitate acid (PA) and its cellular receptor CD36 in the progression of GC.
methodsImmunohistochemical (IHC) staining was performed to detect CD36 expression in GC tissues and its clinical significance was determined statistically. CD36 over-expression and knock-down expression cell models were developed and tested in vitro. Wound-healing assays, migration assays, and invasion assays were performed and peritoneal implants into nude mice were done to assess the biological effects of PA and CD36. The underlying mechanisms were investigated using western blot, immunofluorescence (IF), quantitative real-time PCR (qRT-PCR) and antibody blocking assays.
resultsPA promoted the metastasis of GC by phosphorylation of AKT, which facilitated the nuclear localization of β-catenin through inactivation of GSK-3β via phosphorylation. This tumor-promoting effect of PA was mediated by CD36, a cell surface receptor of fatty acids (FAs). The higher the CD36 expression levels in GC tissues correlated with the poorer the prognosis of patients according to the TCGA database, the GEO database and our own clinical data.
conclusionsOur experiments established CD36 as a key mediator of FA-induced metastasis of GC via the AKT/GSK-3β/β-catenin signaling pathway. CD36 might, therefore, constitute a potential therapeutic target for clinical intervention in GC.
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