TY - JOUR
T1 - Latent membrane protein-1 of Epstein-Barr virus induces the expression of B-cell integration cluster, a precursor form of microRNA-155, in B lymphoma cell lines
AU - Rahadiani, Nur
AU - Takakuwa, Tetsuya
AU - Tresnasari, Kristianti
AU - Morii, Eiichi
AU - Aozasa, Katsuyuki
N1 - Funding Information:
This study was supported by grants from the Ministry of Education, Culture, Sports, Science, and Technology.
PY - 2008/12/12
Y1 - 2008/12/12
N2 - miR-155, a microRNA, and its precursor form, B-cell integration cluster (BIC), are involved in tumor growth. Epstein-Barr virus (EBV)-associated malignancies are categorized into three types, based on their latent gene expression pattern: latency I, II, and III. In the present study, we found that infection with EBV increased the expression of BIC; in addition, substantial expression of BIC/miR-155 was detected in latency III-, but not in latency I-type cells. In comparison, latent membrane protein-1 (LMP1) was expressed in latency III-type cells. When LMP1 was over-expressed, BIC expression increased, indicating LMP1 mediates BIC expression. LMP1 is a membrane-associated protein known to activate signaling pathways. With the use of pathway inhibitors, we found that LMP1-induced strong BIC expression, primarily through NF-κB and p38/MAPK pathways. These results suggest that BIC/miR-155 play a role in lymphomagenesis through NF-κB and p38/MAPK pathways in response to activation by EBV LMP1.
AB - miR-155, a microRNA, and its precursor form, B-cell integration cluster (BIC), are involved in tumor growth. Epstein-Barr virus (EBV)-associated malignancies are categorized into three types, based on their latent gene expression pattern: latency I, II, and III. In the present study, we found that infection with EBV increased the expression of BIC; in addition, substantial expression of BIC/miR-155 was detected in latency III-, but not in latency I-type cells. In comparison, latent membrane protein-1 (LMP1) was expressed in latency III-type cells. When LMP1 was over-expressed, BIC expression increased, indicating LMP1 mediates BIC expression. LMP1 is a membrane-associated protein known to activate signaling pathways. With the use of pathway inhibitors, we found that LMP1-induced strong BIC expression, primarily through NF-κB and p38/MAPK pathways. These results suggest that BIC/miR-155 play a role in lymphomagenesis through NF-κB and p38/MAPK pathways in response to activation by EBV LMP1.
KW - BIC/miR-155
KW - EB virus
KW - LMP1
KW - Lymphoma
UR - http://www.scopus.com/inward/record.url?scp=55549137039&partnerID=8YFLogxK
U2 - 10.1016/j.bbrc.2008.10.007
DO - 10.1016/j.bbrc.2008.10.007
M3 - Article
C2 - 18926796
AN - SCOPUS:55549137039
SN - 0006-291X
VL - 377
SP - 579
EP - 583
JO - Biochemical and Biophysical Research Communications
JF - Biochemical and Biophysical Research Communications
IS - 2
ER -