ArticleOncogene2018
Adipocyte-induced CD36 expression drives ovarian cancer progression and metastasis.
Article in Oncogene, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 339 papers, 1 of them a synthesis that pooled it.
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Who cites it
339 citing papers in PubMed, 1 synthesis or guideline pooled it, 512 citations in OpenAlex.
- Preclinical efficacy and mechanisms of statin-loaded polymeric nanocapsules: a meta-analysis of tumor lipid metabolism inhibition.Scientific reports · 2025Pooled it
- Extracellular vesicle lipidomics liquid biopsy reveals systemic and tumor microenvironment metabolic reprogramming in ovarian cancer.Molecular oncology · 2026Article
- Subtype-specific mechanisms of lipid metabolism in gynecological malignancies and novel targeted intervention strategies (Review).Oncology letters · 2026Review
- Dyslipidaemias in cancer patients.European heart journal · 2026Review
- Glucose-induced histone lactylation confers metformin resistance in colorectal cancer stem cells.Nature communications · 2026Article
- Lipid metabolic reprogramming in ovarian cancer: molecular mechanisms and therapeutic implications.Medical molecular morphology · 2026Review
- THBS2: the key hub linking breast cancer stroma, immunity, and therapeutic response.Clinical & experimental metastasis · 2026Review
- Peritoneal ovarian cancer growth in the omentum proceeds independently of mature adipocytes.Nature communications · 2026Article
- Exosome-Associated Proteins as Mediators and Biomarkers of Ovarian Cancer Dissemination.Biomolecules · 2026Review
- CD36 as a Context-Dependent Regulator of Metabolic Switching in Acute and Chronic Hypoxia.Biomolecules · 2026Review
- The lethal symbiont: exploring the pathophysiology of cancer.Physiological reviews · 2026Review
- Lipids in ovarian cancer ascites impair T cell activation by disrupting TCR dynamics.Nature metabolism · 2026Article
- Reverse cardio-oncology: neuroendocrine axis activation and cardiovascular-disease-derived factors synergistically remodel the tumor microenvironment.Cellular oncology (Dordrecht, Netherlands) · 2026Review
- NEK1 Promotes Ovarian Cancer Progression via p53 Suppression While Enhancing Sensitivity to Genotoxic Therapy.Current issues in molecular biology · 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
- Peritumoural adipose tissue promotes ferroptosis resistance by 3-hydroxykynurenine-mediated suppression of ferritinophagy.Nature cell biology · 2026Article
- Metabolic networks in the tumor microenvironment: roles of amino acid and lipid metabolism pathways in cancer progression and therapy.Experimental & molecular medicine · 2026Review
- Inhibiting stearoyl-CoA desaturase suppresses bone metastatic prostate cancer by modulating cellular stress, mTOR signaling, and DNA damage response.FEBS letters · 2026Article
- PCDHGC3 silencing promotes clear cell renal cell carcinoma metastasis via mTOR/HIF2α activation, lipid metabolism rewiring, and ferroptosis evasion.Cell death & disease · 2026Article
279 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
13 authors at 5 institutions in 2 countries.
Funding
Abstract
Ovarian cancer (OvCa) is characterized by widespread and rapid metastasis in the peritoneal cavity. Visceral adipocytes promote this process by providing fatty acids (FAs) for tumour growth. However, the exact mechanism of FA transfer from adipocytes to cancer cells remains unknown. This study shows that OvCa cells co-cultured with primary human omental adipocytes express high levels of the FA receptor, CD36, in the plasma membrane, thereby facilitating exogenous FA uptake. Depriving OvCa cells of adipocyte-derived FAs using CD36 inhibitors and short hairpin RNA knockdown prevented development of the adipocyte-induced malignant phenotype. Specifically, inhibition of CD36 attenuated adipocyte-induced cholesterol and lipid droplet accumulation and reduced intracellular reactive oxygen species (ROS) content. Metabolic analysis suggested that CD36 plays an essential role in the bioenergetic adaptation of OvCa cells in the adipocyte-rich microenvironment and governs their metabolic plasticity. Furthermore, the absence of CD36 affected cellular processes that play a causal role in peritoneal dissemination, including adhesion, invasion, migration and anchorage independent growth. Intraperitoneal injection of CD36-deficient cells or treatment with an anti-CD36 monoclonal antibody reduced tumour burden in mouse xenografts. Moreover, a matched cohort of primary and metastatic human ovarian tumours showed upregulation of CD36 in the metastatic tissues, a finding confirmed in three public gene expression data sets. These results suggest that omental adipocytes reprogram tumour metabolism through the upregulation of CD36 in OvCa cells. Targeting the stromal-tumour metabolic interface via CD36 inhibition may prove to be an effective treatment strategy against OvCa metastasis.
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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.