Epstein-Barr Virus 감염 Burkitt’s Lymphoma 세포주에 Mitomycin C 처리 시 종양유전자 발현
Expression of Cancer-Related Genes in Epstein Barr Virus-Infected Burkitt´s Lymphoma Cell Line Treated with Mitomycin C
염범우, 김철환, 김인선, 김민경, 이대일, 박설희,
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염범우 ( Yeom Bom-Woo )
고려대학교 의과대학 병리학교실
김철환 ( Kim Chul-Hwan )
고려대학교 의과대학 병리학교실
김인선 ( Kim In-Sun )
고려대학교 의과대학 병리학교실
김민경 ( Kim Min-Kyung )
고려대학교 의과대학 병리학교실
이대일 ( Lee Da-Le )
고려대학교 의과대학 병리학교실
박설희 ( Park Seol-Hee )
고려대학교 의과대학 병리학교실
KMID : 0357920010350040271
Abstract
Background: lnfection of Epstein Barr virus （EBV） into B cells drives the infected cells into the cell cycle and frequently results in lymphoblastoil cells. Mitomycln C inhibits DNA synthesis of eplithelial cells as well as lymphoid cells by cross-linking with DNA. Many of the cancer cells have various pathways for escaping the responsiveness to the negative growth-regulatory effects of mitomycin C and gaining the immortalized property. The auther performed a cell culture of an EBV infected Jijoye lymphoma cell line, and compared the cell cycle and cancer related genes between the mitomycin treated-and non-treated group.
Methods: DNA and RNA were extracted from the Jijoye cells; and EBV nuclear antigen （EBNA）-1, 2and latent membrane protein （LMP） of EBV and p53 and p21 mRNA analyse was performed.
Results: Mitomycin C blocked G2/M phase, however, mitomycin did not affect the expression of EBNA-1, 2 and LMP. Mitomycin C also increased the p21 mRNA expression without p53 mRNA increase.
Conclusions: Mitomycin C induces B cell apoptosis by blocking the G2/M phase and by increasing p21 mRNA independent to p53, which reveals the presence of an alternative pathway of p21 induction by mitomycin C in EBV positive lymphoma cells
키워드
Epatein-Barr virus;Mitomycin C;p53;p21;Lymphoma cell
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