Expression of Cancer-Related Genes in Epstein Barr Virus-Infected Burkitt's Lymphoma Cell Line Treated with Mitomycin C.
- Author:
Woo Bom YEOM
1
;
Seol Hee PARK
;
Min Kyung KIM
;
Chul Hwan KIM
;
In Sun KIM
;
Dale LEE
Author Information
1. Department of Pathology, College of Medicine, Korea University, Seoul 152-105, Korea. Yeom BW@kuccnx.korea.ac.kr
- Publication Type:Original Article
- Keywords:
Epstein-Barr virus;
mitomycin C;
p53;
p21;
lymphoma cell
- MeSH:
Apoptosis;
B-Lymphocytes;
Burkitt Lymphoma*;
Cell Culture Techniques;
Cell Cycle;
Cell Line*;
DNA;
Epithelial Cells;
Herpesvirus 4, Human;
Lymphocytes;
Lymphoma;
Membrane Proteins;
Mitomycin*;
RNA;
RNA, Messenger;
United Nations
- From:Korean Journal of Pathology
2001;35(4):271-277
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
BACKGROUND: Infection of Epstein Barr virus (EBV) into B cells drives the infected cells into the cell cycle and frequently results in lymphoblastoid cells. Mitomycin C inhibits DNA synthesis of epithelial 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, 2 and 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
