ABSTRACT
Objective To evaluated the role of wt-P53 protein in telomerase regulation in keloid fibroblasts(KFBs). Methods The fibroblasts were derived from human keloid tissue which was proved by pathological diagnosis. KFBs were divided into 2 groups, the transfection group and the untransfection group. wt-p53 gene was transfected into the fibroblasts by adenovirus vectors in the transfection group. The KFBs untransfected with wt-p53 gene served as control (untransfection group). After 48 hours of transfection, the expression of wt-P53 protein was analyzed by both Western blotting and immunofluorescence method, respectively. The telomerase activity was evaluated by TRAP-ELISA after 1-7 days of transfection.Results All the KFBs from 2 groups expressed wt-P53 protein. But the expression level of wt-P53 protein in the transfection group was significantly higher than that in the untransfection group. At the same time of high expression of wt-P53 protein, the telomerase activity of KFBs in transfection group was significantly lower than that in the untransfection group( P＜0.05). Conclusion High level expression of wt-P53 protein can transiently inhibit the telomerase activity of KFBs.
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Objective To study wt-p53 gene's influence on the proliferation of keloid fibroblasts in vitro. Methods wt-p53 gene was transfected into keloid fibroblasts by adenovirus vector. wt-p53 mRNA was analyzed by RT-PCR; wt-p53 protein was evaluated by indirectiy immunofluorescence; The ability of proliferation of keloid fibroblasts was analyzed by cell growing curves; The cell cycle of KFB was checked by FCAS. Results The expression of wt-p53 mRNA and protein was obviously higher in the fibroblasts of the experimental group than those of control group; the rate of G_0~G_1 in cell cycle was higher in the fibroblasts of the experimental group than those of control group; at the same time, the rate of G_2~M was lower in fibroblasts of the experimental group than those of control group (P
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Objective To discuss the growth suppressing, apoptosing effect of new type tumor-supressor gene-p33ING1 in stomach cancer cell strain, and to explore new strategies and methods in tumor therapy. Methods The PCDNA3/p33ING1 nuclear expressing microsome was constructed, p33ING1 and wt-p53 were implanted to human stomach cancer cell both and to evaluate the effect of p33ING1 and p53 toward stomach cancer cell and synergism between them. Results The PCDNA3/p33ING1 nuclear expressing microsome was successfully constructed. The human stomach cancer cell strain SSCG-7901 under implantation of p33ING1 and wt-p53 showed a significant decrease in cell growth, the coupling time was delayed, DNA synthetic phase was shortened and G0/G1 phase prolonged. The cell collapse increased. Conclusions Despite of the tumor-inhibiting effect and biochemical activation of p33ING1, it also plays a role with p53 gene in controling growth of stomach cancer cell, inducing cell collapse and hampering cell proliferation cycle. P33ING1 and p53 are synergistic to each other.
ABSTRACT
We have previously shown overexpression of p53 and rearrangement of the p53 gene in AK-5 tumour. In order to study the role of p53 in AK-5 tumourogenicity, we introduced wild-type p53 in AK-5 cells. We have shown suppression of tumourogenicity in AK-5 cells after transfixion with wt p53. In one of the transfected clones 3B4, there was complete loss of tumour forming ability. Clone 3B4 also showed cellular aggregation which correlated well with the higher expression of cell adhesion molecules like fibronectin and hyaluronectin. These observations demonstrate tumour suppression in AK-5 after introduction of wt p53.