ArticleCancers2022
Upregulation of CD36, a Fatty Acid Translocase, Promotes Colorectal Cancer Metastasis by Increasing MMP28 and Decreasing E-Cadherin Expression.
Article in Cancers, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
What it found
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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
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Who cites it
36 citing papers in PubMed, 52 citations in OpenAlex.
- Fatty Acid Metabolism and Hypoxia in the Tumor Microenvironment: Metabolic Adaptation and Clinical Potential in Colorectal Cancer.Biomedicines · 2026Review
- Review
- Understanding the Interplay Between Obesity and Cancer: From Mechanisms to Therapeutic Opportunities.Cancers · 2026Review
- FASN Inhibition Enhances the Efficacy of Chemotherapy in Colorectal Cancer by Inhibiting the DNA Damage Response.Cancer research · 2026Article
- Identification and validation of a Golgi apparatus related gene signature for prognosis prediction and immune microenvironment profiling in colorectal cancer.Discover oncology · 2026Article
- Lipid metabolism as a central driver of immune remodeling and therapeutic vulnerability in metastatic colorectal cancer.Lipids in health and disease · 2026Review
- Mechanisms of fatty acid metabolism in tumor metastasis and targeted therapeutic strategies.Discover oncology · 2026Review
- High INHBB expression in colorectal cancer is associated with poor prognosis and drives malignant phenotypes in tumor cells.Biology direct · 2026Article
- Lipids grease the chain of cancer progression.Trends in cancer · 2026Review
- Research Advances in Nanodrugs Targeting Lipid Metabolism Reprogramming for Colorectal Cancer Therapy.International journal of nanomedicine · 2026Review
- 15,16-Dihydrotanshinone I, a novel β-catenin-targeting inhibitor that inhibits its nuclear translocation and reduces downstream CD36 expression in cancer.Journal of translational medicine · 2025Article
- Identification of New CD36 Antagonists by Structure-Based Virtual Screening.Chemical biology & drug design · 2025Article
- Lipid metabolic reprogramming in colorectal cancer: Insights to mechanisms and therapeutics.World journal of gastrointestinal oncology · 2025Review
- PLA2 driven lipid signaling drives ARMS tumorigenic cell properties.Cell communication and signaling : CCS · 2025Article
- Aspirin impedes non-small cell lung cancer development via fine-tuning the CD36 localization regulated by GPIHBP1.Translational lung cancer research · 2025Article
- An Insight into Prognostic Impact of TIPE2 & CD36 Immunohistochemical Expression in Urothelial Carcinoma.Iranian journal of pathology · 2025Article
- Lipid metabolic reprogramming in colorectal cancer: mechanisms and therapeutic strategies.Frontiers in immunology · 2025Review
- Roles of posttranslational modifications in lipid metabolism and cancer progression.Biomarker research · 2024Review
- Factors Determining Epithelial-Mesenchymal Transition in Cancer Progression.International journal of molecular sciences · 2024Review
- Fatty acid metabolism-related enzymes in colorectal cancer metastasis: from biological function to molecular mechanism.Cell death discovery · 2024Review
Corrections and comments
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
Abstract
Altered fatty acid metabolism continues to be an attractive target for therapeutic intervention in cancer. We previously found that colorectal cancer (CRC) cells with a higher metastatic potential express a higher level of fatty acid translocase (CD36). However, the role of CD36 in CRC metastasis has not been studied. Here, we demonstrate that high expression of CD36 promotes invasion of CRC cells. Consistently, CD36 promoted lung metastasis in the tail vein model and GI metastasis in the cecum injection model. RNA-Seq analysis of CRC cells with altered expression of CD36 revealed an association between high expression of CD36 and upregulation of MMP28, a novel member of the metallopeptidase family of proteins. Using shRNA-mediated knockdown and overexpression of CD36, we confirmed that CD36 regulates MMP28 expression in CRC cells. siRNA-mediated knockdown of MMP28 decreases invasion of CRC cells, suggesting that MMP28 regulates the metastatic properties of cells downstream of CD36. Importantly, high expression of MMP28 leads to a significant decrease in active E-cadherin and an increase in the products of E-cadherin cleavage, CTF1 and CTF2. In summary, upregulation of CD36 expression promotes the metastatic properties of CRC via upregulation of MMP28 and an increase in E-cadherin cleavage, suggesting that targeting the CD36-MMP28 axis may be an effective therapeutic strategy for CRC 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.