Abstract | BACKGROUND & OBJECTIVE: METHODS: Proliferation of MCF-7 cells stimulated by vMIP-II of different concentrations (10, 50, 100, 500, and 1 000 ng /ml) was detected by MTT assay, clone formation rate was assessed by agar clone assay. Adhesion and chemotaxis assays were also used to evaluate the effect of vMIP-II on MCF-7 cells in different steps of metastasis. RESULTS: MCF-7 cells treated with vMIP-II of a series of concentrations for 72 h showed no proliferation change (P >0.05). vMIP-II (50-1 000 ng /ml) suppressed colony formation of MCF-7 cells in a concentration-dependent manner. After MCF-7 cells treated with 300 ng/ml of vMIP-II for different time (0, 0.5, 2, and 6 h), inhibition peak of cell adherence to fibronectin (FN) and Matrigel was observed. The number of migration was low in MCF-7 cells in the presence of vMIP-II of 500 ng/ml (24+/-10) was lower than that of control MCF-7 cells (60+/-9) (P< 0.05). CONCLUSIONS: The clone formation rate of MCF-7 cells may negatively correlates with the concentration of vMIP-II. vMIP-II may inhibit MCF-7 cells adhesion to FN and Matrigel, and suppress chemotactic activity of MCF-7 cells toward extracts of human lung protein.
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Authors | Fu-Jin Liu, Han-Xiao Sun |
Journal | Ai zheng = Aizheng = Chinese journal of cancer
(Ai Zheng)
Vol. 23
Issue 11
Pg. 1283-7
(Nov 2004)
China |
PMID | 15522174
(Publication Type: English Abstract, Journal Article)
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Chemical References |
- Chemokines
- Drug Combinations
- Fibronectins
- Laminin
- Proteoglycans
- Receptors, CXCR4
- vMIP-II
- matrigel
- Collagen
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Topics |
- Breast Neoplasms
(metabolism, pathology)
- Cell Adhesion
(drug effects)
- Cell Line, Tumor
- Cell Migration Inhibition
- Cell Movement
(drug effects)
- Cell Proliferation
(drug effects)
- Chemokines
(administration & dosage, pharmacology)
- Chemotaxis
(drug effects)
- Collagen
(metabolism)
- Dose-Response Relationship, Drug
- Drug Combinations
- Female
- Fibronectins
(metabolism)
- Humans
- Laminin
(metabolism)
- Neoplasm Metastasis
- Proteoglycans
(metabolism)
- Receptors, CXCR4
(antagonists & inhibitors)
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