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
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 i...
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Veröffentlicht in: | Biochemical and biophysical research communications 2008-12, Vol.377 (2), p.579-583 |
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Sprache: | eng |
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Zusammenfassung: | 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. |
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ISSN: | 0006-291X 1090-2104 |
DOI: | 10.1016/j.bbrc.2008.10.007 |