microRNA 28 controls cell proliferation and is down-regulated in B-cell lymphomas

• DOI: 10.1073/pnas.1322466111
• Publication Date: 2014-05-20T02:36:03Z
• Authors: Christof Schneider; Manu Setty; Antony B. Holmes; Roy L. Maute; Christina S. Leslie; Lara Mussolin; Angelo Rosolen; Riccardo Dalla-Fa...; Katia Basso
• Keywords: B-Lymphocytes; 0303 health sciences; Lymphoma, B-Cell; Carcinogenesis; MAP Kinase Signaling System; Genes, myc; Down-Regulation; Nuclear Proteins; Cell Cycle Proteins; Germinal Center; Burkitt Lymphoma; DNA-Binding Proteins; Gene Expression Regulation, Neoplastic; MicroRNAs; 03 medical and health sciences; Cell Transformation, Neoplastic; Cell Line, Tumor; Humans; RNA Processing, Post-Transcriptional; Adaptor Proteins, Signal Transducing; Cell Proliferation; Transcription Factors

Significance The majority of non-Hodgkin B-cell lymphomas arise from the malignant transformation of germinal center B cells. The molecular pathogenesis of these malignancies is not fully understood. Although a number of oncogenes and tumor suppressors have been identified among protein-coding genes, the role of microRNAs during lymphomagenesis remains largely unexplored. Our results identify a role for microRNA 28 (miR-28) in normal and malignant germinal center B cells. These data provide new insights on the microRNA-mediated posttranscriptional regulation occurring in normal germinal center B cells as well as during lymphomagenesis. In addition, the identification of a cross talk between miR-28 and v-myc avian myelocytomatosis viral oncogene homolog extends the relevance of our observations to a wide variety of malignancies.