Methyl-β-cyclodextrin inhibits cell growth and cell cycle arrest via a prostaglandin E(2) independent pathway
Open accessAbstract
Methyl-beta-cyclodextrin, a cyclic oligosaccharide known for its interaction with the plasma membrane induces several events in cells including cell growth and anti-tumor activity. In this study, we have investigated the possible role of cyclooxygenase 2 (COX-2) in cell growth arrest induced by methyl-beta-cyclodextrin in Raw264.7 macrophage cells. Methyl-beta-cyclodextrin inhibited cell growth and arrested the cell cycle, and this cell cycle arrest reduced the population of cells in the S phase, and concomitantly reduced cyclin A and D expressions. Methyl-beta-cyclodextrin in a dose- and time-dependent manner, also induced COX-2 expression, prostaglandin E(2) (PGE(2)) synthesis, and COX-2 promoter activity. Pretreatment of cells with NS398, a COX-2 specific inhibitor completely blocked PGE(2) synthesis induced by methyl-beta-cyclodextrin, however inhibition on cell proliferation and cell cycle arrest was not effected, suggesting non-association of COX-2 in the cell cycle arrest. These results suggest that methyl-beta-cyclodextrin induced cell growth inhibition and cell cycle arrest in Raw264.7 cells may be mediated by cyclin A and D1 expression.
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Methyl β-CD inhibits cell growth and induces cell cycle arrest via a prostaglandin E2 independent pathway in Raw264.7 macrophage cells.
“it has been reported that methyl β-CD inhibits cell growth and induces cell cycle arrest via a prostaglandin E2 independent pathway in Raw264.7 macrophage cells [67].”
From The Effect of Lycopene Preexposure on UV‐B‐Irradiated Human Keratinocytes (2016) · cites this paper as [67]
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Cited by
Sorted by citations
The Effect of Lycopene Preexposure on UV‐B‐Irradiated Human Keratinocytes
Ascenso, A., Pedrosa, T., Pinho, S., Pinho, F., Oliveira, J. M. P. F. D., Cabral Marques, H., Oliveira, H., Simões, S., & Santos, C. (2016) · Oxidative Medicine and Cellular Longevity · doi:10.1155/2016/8214631 · Cited by 57 · see citing works
- Authors
- Choi, Y.-A., Chin, B. R., Rhee, D. H., Choi, H.-G., Chang, H.-W., Kim, J.-H., & Baek, S.-H.
- Affiliations
- Yeungnam University College (KR)
- Yeungnam University (KR)
- Corresponding author
- Choi, Han-Gon
- Venue
- Experimental & Molecular Medicine
- Published
- 2004-02-01
- Volume
- 36
- Issue
- 1
- Pages
- 78-84
- ISSN
- 1226-3613 (ISSN-L)
- 2092-6413
- OpenAlex
- W1980813466
- Cited by
- 23
- References
- 32
- Citations by year
- 2025: 2 · 2024: 2 · 2023: 2 · 2022: 1 · 2020: 1 · 2019: 1 · 2018: 2 · 2016: 1 · 2015: 1
- FWCI
- 1.05
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- Experimental & Molecular Medicine (publishedVersion, cc-by-nc)
- PubMed (publishedVersion)
- Funders
- Yeungnam University
- Topics
- Health Sciences › Medicine › Pharmacology › Inflammatory mediators and NSAID effects
- Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Peroxisome Proliferator-Activated Receptors
- Keywords
- methyl-β-cyclodextrin, cell cycle arrest, cell growth inhibition, cyclooxygenase-2, prostaglandin E2, cyclin A, cyclin D1, S phase, macrophages, RAW 264.7 macrophages, NS-398, antiproliferative activity
- MeSH terms
- Animals, Cell Cycle, Cell Line, Dose-Response Relationship, Drug, Isoenzymes, Macrophages, Prostaglandin-Endoperoxide Synthases, Dinoprostone, beta-Cyclodextrins, Cell Proliferation, Mice, Cyclooxygenase 2
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