| To study the mechanism of occurrence, development, infiltration and metastasis in colorectal cancer is the focus viewpoint in oncology. In recent years, fibroblast growth factor ( FGF ) has been found as a kind of polypeptide growth factor which is widely spreading in vivo, its biology activity is close correlation with neoplasm growth. The acidic fibroblast growth factor (aFGF) and basic fibroblast growth factor ( bFGF) are two mainly fibroblast growth factors in the family members. aFGF and bFGF have similar structure and function and they act on the same receptor. FGF receptor (FGFR) is a kind of type IV stride membrane receptor which has self phosphoric acid activity. It has 4 types: FGFR1, FGFR2, FGFR3 and FGFR4, they are all belong to tyrosine protein kinase (TPK) receptor and FGFR1 is taking up 85 percent. Every kinds of FGFR can conjugate with different kinds of FGF members and different kinds of FGFR has its tissue specificity. The study of FGF in colorectal cancer was mostly focused on bFGF, aFGF has sparsely been seen update. So we study the expression of aFGF, bFGF and FGFR, in colorectal cancer tissue by RT -PCR technique.Tyrosine protein kinase (TPK) is a kind of protein kinase which catalysis the tyrosine residue phosphorylation. The TPK activity will be induced when FGF and its receptor conjugated. The substrate protein will be phosphorylated and then cause cell cleavage and proliferation. In this study, we use the TPK specific inhibitor genistein and observe the inhibition of the proliferation in colorectal cancer cell line CCL229 which has been induced by aFGF or bFGF and ob-serve the cell apoptosis phenomenon, and then to explore the signal transduction in tumor cells and provide the basis of inhibiting the tumor cells proliferation by inhibiting the signal transduction pathway.Signal transduction and controlling is essential for highdegree animals' development and advancement. If disorder, the cell division will become uncontrolled and carcinogenesis happens. Tyrosine protein kinase (TPK) signaling pathway is an important pathway. Many growth factor receptors have TPK activity. Protein kinase C(PKC) is a widespread family of serine/threonine kinase that mediate the cell proliferation and differentiation. Extracellular regulated kinase ( ERK) is one of the mitogen activated protein kinase ( MAPK) family, which can be activated by growth factors, hormone and neurotransmitter and cause malignant conversion. The mechanism of FGF in the colorectal cancer is unknown uptoday. We explore the change of PKC and ERK activity induced by FGF and TPK inhibitor genistein in human colorectal cancer cell line CCL229 and discuss the carcinogenesis and development of colorectal cancer.Materials and Methods1. The expression of aFGF, bFGF and FGFRj in colorectal cancer tissue was evaluated by RT - PCR technique.2. MTT assay was used to determine the suppressive effect of genistein on human colorectal cancer cell line CCL229 induced by aFGF and bFGF. Electron microscope and DNA - ladder electrophoresis were used to observe the cell apoptosis induced by genistein.3. The activity of PKC and ERK in cells induced by different cocentration of aFGF, bFGF and genistein was detected by incorporation of [ r - 32P] - ATP into exogens substrate.Results1. Exprssion of aFGFmRNA, bFGFmRNA and FGFR, mRNA in colorectalcancer.The positive rates aFGF, bFGF and FGFRj in colorectal cancer tissue were 60% ,68% and 64% ,respectively, the positive rates of aFGF, bFGF and FGFRj in the peritumoral tissue were 4% , 8% and 10% , respectively. There was no postive cases in the control group. The expression- levels of aFGFmRNA, bFG-FmRNA and FGFR1 mRNA in Dukes stage C and D were significantly higher than those in Dukes stage A and B (P <0. 05). There were no difference in the differentiated grade ( P > 0.05 ).2. The effect of aFGF, bFGF and genistein on the proliferation of CCL229 cell.aFGF and bFGF could improve the proliferation of CCL229 significantly; the combination of aFGF and bFGF...
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