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Aberrant p16INK4A RNA transcripts expressed in hepatocellular carcinoma cell lines regulate pRb phosphorylation by binding with CDK4, resulting in delayed cell cycle progression

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Author(s)
Jae-We ChoYong-Wook JeongSeung-Wook HanJae-Bok ParkByeong-Churl JangWon-Ki BaekTaeg Kyu KwonJong-Wook ParkSang-Pyo KimMin-Ho SuhSeong-Il Suh
Keimyung Author(s)
Suh, Seong IlKwon, Taeg KyuPark, Jong WookKim, Sang PyoSuh, Min HoJang, Byeong ChurlBaek, Won Ki
Department
Dept. of Molecular Medicine (분자의학)
Dept. of Microbiology (미생물학)
Dept. of Immunology (면역학)
Dept. of Pathology (병리학)
Journal Title
Liver International
Issued Date
2003
Volume
23
Issue
3
Keyword
aberrant RNA transcriptshepatocarcinogenesisp16INK4Apromoter hypermethylation
Abstract
The inactivation of the p16INK4A (p16) gene by promoter hypermethylation has been reported in many human cancers. We previously reported that aberrant p16 RNA transcripts are expressed in hepatocellular carcinoma (HCC) cell lines having hypermethylated p16 promoters. In this study, we investigated the functional roles of aberrant p16 RNA transcripts in HCC cells to elucidate molecular events underlying hepatocarcinogenesis. The aberrant p16 RNA transcripts encoded key peptides (amino acids 84–103) involved in binding with cyclin-dependent kinase (CDK) 4. GST-aberrant p16 fusion proteins were found to interact with endogenous CDK4 in vitro. Furthermore, overexpression of these aberrant p16 RNA transcripts resulted in decreased cell proliferation rate, enlargement of cell shape and reduced level of hyperphosphorylated forms of pRb. Overall, our results suggest that the aberrant p16 RNA transcripts have functions similar to those of wild type p16 in controlling cell cycle.
Keywords:

aberrant RNA transcripts;
hepatocarcinogenesis;
p16INK4A;
promoter hypermethylation
Keimyung Author(s)(Kor)
장병철
백원기
서민호
서성일
권택규
박종욱
김상표
Publisher
School of Medicine
Citation
Jae-We Cho et al. (2003). Aberrant p16INK4A RNA transcripts expressed in hepatocellular carcinoma cell lines regulate pRb phosphorylation by binding with CDK4, resulting in delayed cell cycle progression. Liver International, 23(3), 194–200. doi: 10.1034/j.1600-0676.2003.00821.x
Type
Article
ISSN
1478-3223
Source
https://onlinelibrary.wiley.com/doi/abs/10.1034/j.1600-0676.2003.00821.x
DOI
10.1034/j.1600-0676.2003.00821.x
URI
https://kumel.medlib.dsmc.or.kr/handle/2015.oak/33396
Appears in Collections:
1. School of Medicine (의과대학) > Dept. of Immunology (면역학)
1. School of Medicine (의과대학) > Dept. of Microbiology (미생물학)
1. School of Medicine (의과대학) > Dept. of Molecular Medicine (분자의학)
1. School of Medicine (의과대학) > Dept. of Pathology (병리학)
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