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TSG of NPC (Tumor suppressor genes of nasopharyngeal carcinoma) - (Apr/07/2005 )

Hello. I would like to ask some terms about studying TSG.
1) What are NIH3T3 cells and C17 cells?
2) What are their properties?
3) Why EBV Epstein-Barr virus is related to tumor formation? Is it contributed by its replication mode?



in such cases regarding cell properties, you'll get some useful ones at atcc website.

NIH 3T3 cells are mouse fibroblasts cell line derived from embryo. (ATCC related webpage here

C17 is a retrovirally immortalized neuronal cell line. (PubMed reference here and are a type of migratory brain cell, known as neural progenitor, developed by Evan Snyder, an assistant professor of neurology at Harvard Medical School if i'm not wrong dry.gif...

The litterature and ATCC website(for NIH3T3) will give you the main poperties of these cells.

The Ebstein Barr virus (EBV) is an herpes virus, and was originaly isolated by mr ebstein and barr and has pathogene properties described by dennis burkitt from the burkitt lymphoma epidemilogical study. It transforms the B cells, stay at latent stage in an adult and has defined immortalization properties. Paradoxally, it can immortalize very well in vitro but is silent in humans. The main affection in young adults is mononucleosis. In immunodeficient patients, it provokes tha Kaposi syndrome. Plenty of B and Th cells are raised against it but it is never well eliminated.
this virus express these proteins :
EBNA 1, 2, 3A, 3B, LP, 3C. (Ebst Barr Nuclear antigens)
LMP 1, 2A, 2B
LMP1 is an oncogene
EBNA1 ensures the persistance of viral genome in about 10 to 30 memory B cells.

in fact LMP1 blocks the cell cycle regulationg protein p16.

normally p16 INK4 protein is activated in ultraviolet cell response or during replicative senescence. Its role is to repress CDK4/6_Cyclin D complex.
CDK4/6_Cyclin D complex play a role in stimulating replication at G1/S checkpoint.
Hence, if p16 is blocked, it can not repress CDK:cyc. The result is that CDK:cyc is more active and cell entry in S phase is less controlled.

Sorry for the long answer...

here are some references
Delecluse HJ, and al. The expression of Epstein-Barr virus latent proteins is related to the pathological features of post-transplant lymphoproliferative disorders. Am J Pathol 1995 ; 146 : 1113-20.

Socie G, Kolb B. Malignant diseases after bone marrow transplantation : the case for tumor banking and continued reporting to registries. Bone Marrow Transplantation 1995 ; 16 : 493-5.

Kingma DW, and al. Epstein-Barr virus latent membrane protein-1 oncogene deletions : correlations with a malignancy in Epstein-Barr virus-associated lymphoproliferative disorders and malignant lymphomas. Blood 1996 ; 88 : 242-51.

Naoko Ohtani, and al.Epstein-Barr virus LMP1 blocks p16INK4a-RB pathway by promoting nuclear export of E2F4/5. 2003. The Journal of Cell Biology, Volume 162, Number 2, 173-183


Thanks very much.