Effect and mechanism of action of non-mitogenetic human acidic fibroblast growth factor on the mitogenic activity of the mammary tumor cell.
- Author:
Qing ZHENG
1
;
Fei PENG
;
Xiao-ping WU
;
Zhi-jian SU
;
Xiao-kun LI
Author Information
- Publication Type:Journal Article
- MeSH: 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
- From: Acta Pharmaceutica Sinica 2006;41(3):263-267
- CountryChina
- Language:Chinese
-
Abstract:
AIMTo compare the effects of the non-mitogenetic human acidic fibroblast growth factor (nmhaFGF) and the human acidic fibroblast growth factor (haFGF) on the proliferation and MAPK signal transduction pathway of the malignant tumor cell and to study the clinical safety of nmhaFGF.
METHODSThe 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.
RESULTSThe 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.
CONCLUSIONThe 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.
