Abstract | AIM: METHODS: The mammary tumor cells (MCF-7) were treated with haFGF and nmhaFGF separately. The mitogenic activities of both haFGF and nmhaFGF were detected by MTT method and the cell cycle was analyzed by flow cytometer (FCM). The expression levels of the signal proteins, Grb2 ( growth factor receptor bound 2) and ERK1/2 ( extracellular signal-regulated kinase 1/2), were detected by semi-quantitative Western blotting method. RESULTS: The mitogenic activity of nmhaFGF was obviously lower than that of haFGF. The activity of nmhaFGF was weaker than that of the haFGF. The ratio of G1/G0, G2/M of haFGF was markedly lower than that of nmhaFGF and control group, and was reverse in S phase. The expression levels of both Grb2 and ERK1/2 of the nmhaFGF treated group were lower than that of the haFGF treated group and approaching the control group. CONCLUSION: The mitogenic activity of the nmhaFGF decreased remarkably. Its mechanism probably via down-regulation of the expression of the signal moleculars, MAPK-ERK1/2 and Grb2.
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Authors | Qing Zheng, Fei Peng, Xiao-ping Wu, Zhi-jian Su, Xiao-kun Li |
Journal | Yao xue xue bao = Acta pharmaceutica Sinica
(Yao Xue Xue Bao)
Vol. 41
Issue 3
Pg. 263-7
(Mar 2006)
ISSN: 0513-4870 [Print] China |
PMID | 16759000
(Publication Type: English Abstract, Journal Article, Research Support, Non-U.S. Gov't)
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Chemical References |
- GRB2 Adaptor Protein
- GRB2 protein, human
- Fibroblast Growth Factor 1
- Mitogen-Activated Protein Kinase 1
- Mitogen-Activated Protein Kinase 3
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Topics |
- Breast Neoplasms
(metabolism, pathology)
- Cell Cycle
(drug effects)
- Cell Line, Tumor
- Down-Regulation
- Female
- Fibroblast Growth Factor 1
(genetics, pharmacology)
- GRB2 Adaptor Protein
(metabolism)
- Humans
- Mitogen-Activated Protein Kinase 1
(metabolism)
- Mitogen-Activated Protein Kinase 3
(metabolism)
- Mitosis
(drug effects)
- Mutation
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