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- Publisher
- Wolters Kluwer Health
- Copyright
- Copyright © 2021 Wolters Kluwer Health, Inc. All rights reserved.
- ISSN
- 0959-4973
- eISSN
- 1473-5741
- DOI
- 10.1097/cad.0000000000001036
- Publisher site
- See Article on Publisher Site
Abstract
Caveolin-1 (CAV-1) can extensively regulate lipid transportation, cell growth and cell death. In the present study, we revealed a novel function of CAV-1 in inhibiting glycosylation of other molecules in murine breast cancer cell line. After the silencing of CAV-1, we found that the mRNA and protein expressions of cluster of differentiation 147 (CD147) and its related molecules (MCT4, matrix metalloproteinase MMP2 and MMP9) increased in the breast cancer cells. Meanwhile, the migration and invasion of the breast cancer cells were significantly enhanced assessed by cell wound healing experiment and transwell assays. Further, the gelatin zymography and lactate assay in the cells also showed the strengthened enzyme activity of MMP9 and the increased extracellular lactate concentration, respectively, after the silencing of CAV-1. Notably, the glycosylation level of CD147 overtly increased after the inhibition of CAV-1 detected by Western Blot analysis, whereas upregulation of CAV-1 did the opposite. Therefore, the findings suggest that the downregulation of CAV-1 can promote breast cancer cell progression probably by highly glycosylated CD147.
Journal
Anti-Cancer Drugs – Wolters Kluwer Health
Published: Jun 9, 2021