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사람의 간암 세포주에서 p53 유전자의 기능과 p21^(CIP1) 유전자 발현의 상관관계에 관한 연구
조혜성,임인경 아주대학교 의과학연구소 1996 아주의학 Vol.1 No.1
Expression of p21^(CIP1) gene has been known to be regulated by p53. We have examined whether basal expression of p21^(CIP1) is directly correlated to the status of p53 gene expression in seven human hepatoma cell lines. Six hepatoma cell lines except Hep3B expressed significant amount of p53 and Rb transcripts. However, only three of the six cell lines(HepG2, SK-HEP-1, HT-17) showed detectable basal expression of p21^(CIP1) transcripts, whereas three other Hub cell lines(Huhl, 4 and 7) originated from Japan did not. Neither p21^(CIP1) nor p53 transcripts were observed in the Hep3B cell line. There, was a considerable correlation between the status of functional p53 and p21^(CIP1) gene expression in these hepatoma cells, since loss of p21^(CIP1) gene expression was observed in the Huh7 cells which have mutated p53 and in the Huhl and Huh4 cells which have HBV containing HBX gene. Treatment of HepG2 hepatoma cells with 25 nM testosterone resulted in higher mitogenic activities by the ³H-thymidine incorporation assay. However, expression of p21^(CIP1) gene did not seem to be involved in mitogenic enhancement by testosterone in these cells.
Jin, Yoon Mi,Lee, Jae-Ho,Cho, Hyeseong 아주대학교 1997 아주의학 Vol.2 No.1
Background/aims : Hepatocellular carcinoma is frequently associated with hepatitis B virus infection and HBx protein is suspected to be the main cause of hepatitis B virus related hepatocellular carcinoma. But little is known about the time of the HBx protein expression during hepatocarcinogenesis. These issues, therefore, are addressed in this article. Methods : We examined HBx protein expression in the chronic active hepatitis, cirrhosis and hepatocellular carcinoma by the immunohistochemical method. Results : Among the patients with chronic active hepatitis, four (80%) were HBx protein positive in hepatocytes. In contrast, only one (6%) out of 16 liver specimens with hepatocellular carcinoma showed positivity for HBx protein, whereas four (25%) of suirounding cmhotic tissues showed HBx protein positivity. Thus, differential expression of HBx protein was observed in the livers during hepatocarcinogenesis. HBx protein was expressed mostly in the cytoplasm of hepatocytes. We also examined p53 protein and p21^(WAF1) protein expression in some of the hepatocellular carcinoma. P53 protein was found only in the nucleus of hepatocellular carcinoma cells (38%), and p21^(WAF1)' protein was also detected in some hepatocellular carcinoma tissues irrespective of HBx protein and/or p53 protein expression. Conclusions : These findings suggest that the HBx protein is expressed in the early stage of hepatitis B virus related hepatocarcinogenesis.
Transcriptional regulation and chromatin dynamics at DNA double-strand breaks
Min Sunwoo,Ji Jae-Hoon,Heo Yungyeong,Cho Hyeseong 생화학분자생물학회 2022 Experimental and molecular medicine Vol.54 No.-
In eukaryotic cells, DNA damage can occur at any time and at any chromatin locus, including loci at which active transcription is taking place. DNA double-strand breaks affect chromatin integrity and elicit a DNA damage response to facilitate repair of the DNA lesion. Actively transcribed genes near DNA lesions are transiently suppressed by crosstalk between DNA damage response factors and polycomb repressive complexes. Epigenetic modulation of the chromatin environment also contributes to efficient DNA damage response signaling and transcriptional repression. On the other hand, RNA transcripts produced in the G1 phase, as well as the active chromatin context of the lesion, appear to drive homologous recombination repair. Here, we discuss how the ISWI family of chromatin remodeling factors coordinates the DNA damage response and transcriptional repression, especially in transcriptionally active regions, highlighting the direct modulation of the epigenetic environment.
Park, Sun-Yi,Kim, Sujeong,Cho, Hyeseon,Kwon, Soon-Hwan,Chae, Sunyoung,Kang, Dongmin,Seong, Yeon-Sun,Cho, Hyeseong Landes Bioscience 2009 Cell cycle Vol.8 No.11
<P>The role of BubR1 has been established mainly in mitosis as an essential mitotic checkpoint protein although it is expressed throughout the cell cycle. To explore a possible role of BubR1 in regulating the G(2) phase of cell cycle, we have employed siRNA-mediated hBubR1 knockdown in HeLa cells. Here, we demonstrate that reducing BubR1 levels during the G(2) phase causes accelerated mitotic entry. As expected, BubR1 depletion leads to degradation of cyclin B(1) in the G(2) phase. Intriguingly, cyclin B(1) is prematurely targeted to centrosomes appearing at early G(2) phase in BubR1-depleted cells despite its low levels. This is in contrast to control cells where cyclin B(1) appears at the centrosomes in early prophase based on cell cycle-specific localization of CENP-F. Furthermore, cyclin B/Cdk1 kinase activity in early G(2) is aberrantly high in BubR1-depleted cells. Together, our results indicate that hBubR1 depletion triggers premature centrosomal localization of cyclin B(1) probably leading to premature mitotic entry. This study is the first to suggest a role of hBubR1 in controlling centrosome targeting of cyclin B(1) and timing of mitotic entry.</P>