Journal of Korean Neurosurgical Society
- 제29권4호
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- Pages.471-476
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- 2000
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- 2005-3711(pISSN)
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- 1598-7876(eISSN)
사람의 신경교종 세포주에서 아데노바이러스 벡터를 이용한 p16/INK4a 유전자 전달에 의한 종양성장 억제
Growth Suppression by Adenovirus-mediated Gene Transfer of p16/INK4a in Glioma Cell Lines
- 김미숙 (원자력병원 세포생물학연구실) ;
- 권희충 (원자력병원 분자종양학연구실) ;
- 강희석 (원자력병원 세포생물학연구실) ;
- 박인철 (원자력병원 세포생물학연구실) ;
- 이창훈 (원자력병원 신경외과) ;
- 김창민 (원자력병원 분자종양학연구실) ;
- 이춘택 (서울대학교 의과대학 내과학교실) ;
- 홍석일 (원자력병원 세포생물학연구실) ;
- 이승훈 (원자력병원 신경외과)
- Kim, Mi-Suk (Department of Laboratory of Cell Biology, Korea Cancer Center Hospital) ;
- Kwon, Hee-Chung (Department of Laboratory of Molecular Oncology, Korea Cancer Center Hospital) ;
- Kang, Hee-Seog (Department of Laboratory of Cell Biology, Korea Cancer Center Hospital) ;
- Park, In-Chul (Department of Laboratory of Cell Biology, Korea Cancer Center Hospital) ;
- Rhee, Chang-Hun (Department of Neurosurgery, Korea Cancer Center Hospital) ;
- Kim, Chang-Min (Department of Laboratory of Molecular Oncology, Korea Cancer Center Hospital) ;
- Lee, Choon-Taek (Department of Internal Medicine, Seoul National University, College of Medicine) ;
- Hong, Seok-Il (Department of Laboratory of Cell Biology, Korea Cancer Center Hospital) ;
- Lee, Seung-Hoon (Department of Neurosurgery, Korea Cancer Center Hospital)
- 투고 : 1999.08.09
- 심사 : 1999.11.16
- 발행 : 2000.04.28
초록
Objective : p16/INK4a, a kind of tumor suppressor genes, encodes a specific inhibitor of the cyclin D-dependent kinases CDK4 and CDK6. This prevents the association of CDK4 with cyclin D1, and subsequently inhibits phosphorylation of retinoblastoma tumor suppressor protein(pRb), thus preventing exit from the G1 phase. According to previous reports, over 50% of glioma tissue and 80% of glioma cell lines have been demonstrated inactivation of p16/INK4a gene. The purpose of this study was to determine whether recombinant adenovirus-p16 virus is a suitable candidate for gene replacement therapy in cases of glioma. Methods : Three human glioma cell lines(U251MG, U87MG and U373MG) that express mutant p16 protein were used. Replication-deficient adenovirus was utilized as an expression vector to transfer exogenous p16 cDNA into the cells ; control cells were infected with the Ad-