ArticleOncogenesis2018
CD36 plays a critical role in proliferation, migration and tamoxifen-inhibited growth of ER-positive breast cancer cells.
Article in Oncogenesis, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 76 papers.
What it found
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Who cites it
76 citing papers in PubMed, 209 citations in OpenAlex.
- CD36 as a Context-Dependent Regulator of Metabolic Switching in Acute and Chronic Hypoxia.Biomolecules · 2026Review
- Lipids grease the chain of cancer progression.Trends in cancer · 2026Review
- The Lipid Line of Defence: Monounsaturated Fatty Acids (MUFAs) in Cancer and Ferroptosis.Oxidative medicine and cellular longevity · 2026Review
- Elevated CD36 drives lymph node metastasis of breast cancer by activating Hippo-YAP signaling-mediated anoikis resistance.Communications biology · 2025Article
- Androgen Receptors Promote Oxidative Phosphorylation and Resistance to Palmitate Lipotoxicity in ER-Mutant Breast Cancer.Endocrinology · 2025Article
- Article
- Association between novel agents targeting proprotein convertase subtilisin/kexin type 9 and cancer incidence.Naunyn-Schmiedeberg's archives of pharmacology · 2025Article
- Identification of New CD36 Antagonists by Structure-Based Virtual Screening.Chemical biology & drug design · 2025Article
- The role of genetics and epigenetics in breast cancer: A comprehensive review of metastasis, risk factors, and future perspectives.Journal of pharmaceutical analysis · 2025Review
- Identification of new selective CD36 inhibitors to potentiate HER2-targeted therapy in HER2-positive breast cancer.Scientific reports · 2025Article
- Colchicine reduces neointima formation and VSMC phenotype transition by modulating SRF-MYOCD activation and autophagy.Acta pharmacologica Sinica · 2025Article
- A metabolic shift to the serine pathway induced by lipids fosters epigenetic reprogramming in nontransformed breast cells.Science advances · 2025Article
- Lipid metabolic reprograming: the unsung hero in breast cancer progression and tumor microenvironment.Molecular cancer · 2025Review
- CD36 inhibition enhances the anti-proliferative effects of PI3K inhibitors in PTEN-loss anti-HER2 resistant breast cancer cells.Cancer & metabolism · 2025Article
- Identification of a metabolic-immune signature associated with prognosis in colon cancer and exploration of potential predictive efficacy of immunotherapy response.Clinical and experimental medicine · 2025Article
- Monocyte-cancer cell fusion is mediated by phosphatidylserine-CD36 receptor interaction and induced by ionizing radiation.PloS one · 2025Article
- Targeting CD36-Mediated Lipid Metabolism by Selective Inhibitor-Augmented Antitumor Immune Responses in Oral Cancer.International journal of molecular sciences · 2024Article
- Droplet-based proteomics reveals CD36 as a marker for progenitors in mammary basal epithelium.Cell reports methods · 2024Article
- Mechanisms and significance of entosis for tumour growth and progression.Cell death discovery · 2024Review
- CD36 inhibition reduces non-small-cell lung cancer development through AKT-mTOR pathway.Cell biology and toxicology · 2024Article
16 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 4 institutions in 1 country.
Funding
Abstract
Tamoxifen inhibits estrogen receptor (ER)-positive breast cancer growth while CD36 potentiates cancer metastasis. The effects of CD36 on proliferation/migration of breast cancer cells and tamoxifen-inhibited ER-positive cell growth are unknown. In this study, we correlated the mortality of breast cancer patients to tumor CD36 expression levels. We also found CD36 was higher in ER-rich (MCF-7>T-47D~ZR-75-30) than ER-negative (MDA-MB-231) cells. CD36 siRNA decreased viability and migration of MCF-7 and MDA-MB-231 cells with more potent effects on MCF-7 cells. Inversely, high expressing CD36 enhanced cell growth/migration. Mechanistically, CD36 increased expression of genes responsible for cell proliferation, migration and anti-apoptosis. CD36 also activated ERα and ER-targeted genes for cell cycles, and phosphorylated ERK1/2 (p-ERK1/2). Tamoxifen inhibited CD36 and p-ERK1/2 in ERα-positive but not ERα-negative cells. Reciprocally, inhibition of MCF-7 cell growth by tamoxifen was attenuated by high expressing CD36. CD36, ERα and p-ERK1/2 expression was higher in tamoxifen-resistant MCF-7 (MCF-7/TAMR) cells than normal MCF-7 cells. However, CD36 siRNA restored the capacity of tamoxifen inhibiting MCF-7/TAMR cell growth. CD36 antibody inhibited cell growth and expression of ERα, p-ERK1/2 and CCND1. Therefore, our study unveils a pro-tumorigenic role of CD36 in breast cancer by enhancing proliferation/migration of breast cancer cells while attenuating tamoxifen-inhibited ER-positive cell growth.
Identifiers
What OpenQuestion 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 OpenQuestion graph.