Upregulation of CD36, a fatty acid translocase, promotes colorectal cancer metastasis by increasing MMP28 and decreasing e-cadherin expression
Open accessAbstract
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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BRAFV600E mutation influences the malignancy of CRC by promoting the migration and invasion of CRC cells through activating EMT and downregulating E-cadherin.
“Studies have shown that BRAFV600E mutation influences the malignancy of CRC by promoting the migration and invasion of CRC cells through activating EMT and downregulating E-cadherin [41,42].”
From Inhibition of fatty acid synthase enhances therapeutic efficacy and delays acquired resistance to BRAF-targeted therapy in colorectal cancer (2026) · cites this paper as [42]
The Introduction (section 1; page not available) links E-cadherin loss to EMT and increased CRC cell invasion. The Discussion (section 4; page not available) reports that CD36 and MMP28 are associated with E-cadherin loss in CRC cells, but the cited paper does not attribute this mechanism to BRAFV600E mutation or establish the claimed effect on migration. (LLM, conf=0.86)
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- Authors
- Drury, J., Rychahou, P. G., Kelson, C. O., Geisen, M. E., Wu, Y., He, D., Wang, C., Lee, E. Y., Evers, B. M., & Zaytseva, Y. Y.
- Affiliations
- University of Kentucky (US)
- Corresponding author
- Zaytseva, Yekaterina Y.
- ORCID
- Venue
- Cancers
- Publisher
- MDPI AG
- Published
- 2022-01-05
- Volume
- 14
- Issue
- 1
- Pages
- 252
- ISSN
- 2072-6694 (ISSN-L)
- PMC
- PMC8750155
- OpenAlex
- W4206568533
- Cited by
- 64
- References
- 58
- Citations by year
- 2026: 18 · 2025: 9 · 2024: 13 · 2023: 18 · 2022: 6
- FWCI
- 4.85
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- Cancers (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- UKnowledge (University of Kentucky) (submittedVersion, cc-by)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- National Cancer Institute (NCI R01 CA249734, R01 CA208343)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer, Lipids, and Metabolism
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mechanisms of cancer metastasis
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Protease and Inhibitor Mechanisms
- Keywords
- CD36, fatty acid translocase, colorectal cancer, metastasis, MMP-28, E-cadherin cleavage, tumor invasion, lung metastasis, gastrointestinal metastasis, fatty acid metabolism, therapeutic target
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