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Regulatory role of p53 tumor suppressor gene in the cell cycle G2 check point and celluar senescence
Shin, Deug-Yong 가톨릭 의과학연구원 1998 가톨릭 의과학연구원 국제학술대회 Vol.2 No.-
Here, we show that senescence with specific associated markers can be induced by expression of wild-type p53 in human cancer cells lacking function of this gene. p53-induced senescence caused irreversible cell cycle arrest at G1 and G2/M, and the associated repression of the mitotic cyclins and telomerase activity. These finding demonstrate that wild type p53 can influence the intrinsic senescence program as well as the overlapping pathways of cellular transformation and programmed cell death.
Transcription repression of a CCAAT-binding transcription factor CBF/HSP70 by p53
채희돈,윤진호,신득용 생화학분자생물학회 2005 Experimental and molecular medicine Vol.37 No.5
NF-Y transcription factor binds to CCAAT boxes on promoters of cell cycle regulatory genes such as cdc2, cyclin B, cdc25C, and cyclin A. We previously reported that the DNA binding activity of NF-Y is regulated by p53-p21-cdk2 pathway. CBF/HSP70 was originally identified as a transcription factor binding to the CCAAT box on the hsp70 promoter and mediates transcription repression of hsp70 pro- moter by p53. Recently it was demonstrated that CBF/HSP70 interacts and cooperates with NF-Y. In this study, we found that p53 represses the trans- cription of CBF/HSP70. Since transactivation ability of NF-Y is regulated in a cell cycle-dependent maner, we examined the transcription of CBF/HSP70 during the cell cycle. After synchronization of a human bladder carcinoma cell lacking functional p53 at early S phase, we infect the cells with adenovirus encoding p53. Cels infected with control virus progressed to S and G2 after release from the arrest. In contrast, cells expressing p53 enter S and G2 phases, but arrest at G2/M. The expression of CBF/HSP70 was induced at S/G2 phase in cells infected with a control virus, but kept to be repressed in cells expressing p53. Thus, these results suggest that p53 suppresses the expression of cell cycle regulatory genes though inhibiting both CCAAT binding factors, CBF/HSP70 and NF-Y.
조민경,김영재,신득용,최태생 한국생약학회 2004 생약학회지 Vol.35 No.1
Cell-scattering is a phenotypic change easily observed in most epithelial cells treated with Hepatocyte Growth Factor /scatter Factor (HGF/SF) or phorbol esters (PKC-activators). Recent studies have shown the possibilities to use as therapeuticmaterials of HGF/SF or non tumor promoting phorbol esters for liver disease, cancer and AIDS. In this study, we tested a cell-scattering activity of 534 methanol extracts from plants inhabiting in Korean peninsula using the phenotype-based assay system.Nine Active extracts were detected : Daphne genkwa, Daphne kiusiana, and Aleurites fordii showed high activity (+++),Euphorbia sieboldiana and Rhodotypos scandens showed medium activity (++), Sambucus sieboldiana var. pendula, Catalpabignonioides, Sambucus sieboldiana and Lycoris squamigera showed low activity (+). Furthermore, the effects of these activematerials in the culture cells were investigated with biochemical studies.
Un-Jung Yun,박희동,신득용 대한암학회 2006 Cancer Research and Treatment Vol.38 No.4
Recent studies have suggested that p53 regulates the G2 checkpoint in the cell cycle and this function is required for the maintenance of genomic integrity. In this study, we addressed a role of p53 in escaping from cell cycle G2 arrest following DNA damage.Materials and Methods: Cell cycle checkpoint arrest in the human colon cancer cell line HCT116 and its derivatives carry p53 or p21 deletions, were examined by FACS analysis, immunoprecipitation, Western blot and IP-kinase assay.Results: While the cells with functional p53 were arrested at both the G1 and G2 checkpoints, the p53-deficient cells failed to arrest at G1, but they were arrested at G2. However, the p53-deficient cells failed to sustain G2 checkpoint arrest and they entered mitosis earlier than did the p53-positive cells and so this resulted in extensive cell death. Cdc2 kinase becomes reactivated in p53-deficient cells in association with entry into mitosis, but not in the p53-positive cells. Upon DNA damage, the p21-deficient cells, like the p53-negative cells, not only failed to repress cdk2- dependent NF-Y phosphorylation, but they also failed to repress the expression of such cell cycle G2-regulatory genes as cdc2, cyclin B, RNR-R2 and cdc25C, which have all been previously reported as targets of NF-Y transcription factor.Conclusion: p53 is essential to prevent immature escaping from cell cycle G2 checkpoint arrest through p21-mediated cdk2 inactivation, and this leads to inhibition of cdk2-dependent NF-Y phosphorylation and NF-Y dependent transcription of the cell cycle G2-rgulatory genes, including cdc2 and cyclin B. (Cancer Res Treat. 2006;38:224-228)