Regulation of pri-microRNA BIC transcription and processing in Burkitt lymphomaKluiver, J., van den Berg, A., de Jong, D., Blokzijl, T., Harms, G., Bouwman, E., Jacobs, S., Poppema, S. & Kroesen, B-J. 31-May-2007 In : ONCOGENE. 26, p. 3769-3776 8 p.
Research output: Contribution to journal › Article
BIC is a primary microRNA (pri-miR-155) that can be processed to mature miR-155. In this study, we show the crucial involvement of protein kinase C (PKC) and nuclear factor-kappa B (NF-kappa B) in the regulation of BIC expression upon B-cell receptor triggering. Surprisingly, Northern blot analysis did not reveal any miR-155 expression upon induction of BIC expression in the Burkitt lymphoma-derived Ramos cell line, whereas other microRNAs were clearly detectable. Ectopic expression of BIC in Ramos and HEK293 cells resulted in miR-155 expression in HEK293, but not in Ramos cells, suggesting a specific block of BIC to miR-155 processing in Ramos. In line with the results obtained with Ramos, lack of miR-155 expression after induction of BIC expression was also observed in other Burkitt lymphoma cell lines, indicating a generic and specific blockade in the processing of BIC in Burkitt lymphoma. In contrast, induction of BIC expression in normal tonsillar B cells resulted in very high levels of miR-155 expression and induction of BIC expression in Hodgkin's lymphoma cell lines. It also resulted in elevated levels of miR-155. Our data provide evidence for two levels of regulation for mature miR-155 expression: one at the transcriptional level involving PKC and NF-kappa B, and one at the processing level. Burkitt lymphoma cells not only express low levels of BIC, but also prevent processing of BIC via an, as yet, unknown mechanism.
|Number of pages||8|
|State||Published - 31-May-2007|
- BIC, microRNA-155, Burkitt lymphoma, microRNA processing, B-cell receptor, ADAR, VIRUS-INDUCED LYMPHOMAS, B-CELL LYMPHOMAS, HIGH EXPRESSION, RNA, MIR-155, IDENTIFICATION, MODULATION, ONCOGENES, PRECURSOR, COMPLEX